Paroxysmal dyspnea in Parkinson's disease: Respiratory dyskinesias and autonomic hyperventilation are not the same.

Respiratory complaints are not uncommon in patients with Parkinson's disease (PD). While many are explained by pulmonary and cardiovascular problems unrelated to PD, secondary effects of PD, such as kyphoscoliosis, respiratory muscle rigidity, repeated pneumonias, or side effects of medication such as dyskinesias, there is a small group of patients with paroxysmal dyspnea for whom neither anxiety or other explanation has been found. This Point of View was written to call attention to this neglected, uncommon, but very distressing symptom.

Platypnea-Orthodeoxia Syndrome: A Case of Chronic Paroxysmal Hypoxemia.

A 75-year-old man with chronic (30-year) unexplained paroxysmal hypoxemia presented with postural hypoxemia and desaturation consistent with a clinical manifestation of platypnea-orthodeoxia syndrome. His history included a lack of significant past pulmonary disease, yet with intermittent need for oxygen supplementation. On admission he was found to have an interatrial shunt through a patent foramen ovale. Device closure by percutaneous catheterization led to sustained resolution of symptoms. Platypnea-orthodeoxia syndrome is a rare but important consideration in the differential diagnosis of hypoxemia, as it represents a potentially curable cause of hypoxemia, with missed diagnosis leading to possible patient morbidity if untreated. Even more importantly, an astute and careful history and physical examination are integral to the diagnosis of this rare but likely under-recognized syndrome.

Value of orthopnea, paroxysmal nocturnal dyspnea, and medications in prospective population studies of incident heart failure.

Prospective population studies of incident heart failure (HF) are often limited by difficulties in assembling HF-free cohorts. In this study, public-use copies of the Cardiovascular Health Study (CHS) data sets were used to determine the sensitivity, specificity, and positive and negative predictive values of orthopnea and paroxysmal nocturnal dyspnea (PND), with and without the use of medications used in CHS HF criteria (diuretics plus digoxin or vasodilators), in the diagnosis of prevalent HF and in the assembly of a relatively HF-free population. Of the 5,771 community-dwelling older adults aged > or =65 years, 803 had orthopnea, 660 had PND, 1,075 had either symptom, 388 had both symptoms, 547 were using HF medications, and 4,315 had neither symptom and were not using HF medications. Definite HF was centrally adjudicated in 272 participants. The sensitivity, specificity, and positive and negative predictive values for either orthopnea or PND were 52% (95% confidence interval [CI] 46% to 58%), 83% (95% CI 82% to 84%), 13% (95% CI 11% to 15%), and 97% (95% CI 97% to 98%), respectively, and those for either orthopnea or PND or the use of HF medications were 77% (95% CI 72% to 82%), 77% (95% CI 76% to 79%), 14% (95% CI 13% to 16%), and 99% (95% CI 98% to 99%), respectively. In conclusion, only <20% of those with either orthopnea or PND had definite HF, which limits their usefulness in the diagnosis of prevalent HF in the community. However, nearly 99% (negative predictive value) of those with neither symptom nor using HF medications also did not have HF, which may be useful as a simple and inexpensive tool in assembling relatively HF-free cohorts for prospective population studies of incident HF.

Alveolar membrane conductance decreases as BNP increases during exercise in heart failure. Rationale for BNP in the evaluation of dyspnea.

BACKGROUND: In left ventricular failure (LVF) patients, brain natriuretic peptide (BNP), lung diffusion for carbon monoxide (DLCO), and alveolar-membrane conductance (DM) correlate with LVF severity and prognosis. The reduction of DLCO and DM during exercise reflects pulmonary edema formation. METHODS AND RESULTS: To evaluate, in LVF patients, the correlation between BNP and lung diffusion parameters at rest and during exercise, we studied 17 severe LVF patients, 13 moderate, and 10 normals measuring BNP and lung diffusion parameters before, at the end, and 1 hour after a 10-minute high-intensity constant-workload exercise. At rest, a significant correlation exists between BNP and lung diffusion parameters. Resting BNP, DLCO, and DM correlate with peak oxygen consumption (P < .0001 for all analyses). With exercise, BNP increase is significant (severe LVF 180 +/- 49 pg/mL, moderate 68 +/- 58, normals 18 +/- 12); differently, only in severe LVF, with exercise, DLCO (-1.1 +/- 0.7 mL/mm Hg/min, P < .0001) and DM (-6.4 +/- 2.8, P < .0006) decrease. One hour after exercise, only in severe LVF, BNP is still higher than at rest, while DLCO, DM, and DM/Vc are lower. Significant correlations are observed between BNP and DM changes during exercise and recovery (P < .0001) in severe LVF. CONCLUSIONS: In severe LVF, BNP changes during exercise correlate with simultaneous reductions in DM, suggesting that BNP increase and pulmonary edema formation could be related.

Dyspnoea versus fatigue: additional prognostic information from symptoms in chronic heart failure?

BACKGROUND: In non-heart failure populations, dyspnoea reported by the patient as the reason for stopping an exercise test is associated with a worse prognosis than fatigue. Patients with chronic heart failure (CHF) have exercise limitation due to breathlessness or fatigue, but it is unclear whether one symptom confers an adverse prognosis over the other. METHODS: Consecutive CHF patients underwent exercise testing with metabolic gas exchange. Upon stopping exercise the dominant symptom reported by the patients was recorded. Survival analyses were performed to establish predictors of mortality and relationships between symptoms and objective measures of exercise capacity. RESULTS: Data were analysed on 271 patients (219 men), mean age 67 (10) years, mean left ventricular ejection fraction 32 (8)%, and median follow-up 59 months (interquartile range 38). There were no differences in exercise variables, sex, NYHA class, body mass index and medical therapy between fatigued and dyspnoeic patients. At the censor date 92 (34%) patients had died. Deceased patients had a lower peak oxygen consumption (17.2 (4.6) versus 20.3 (5.6); p=0.0028). Although NYHA class was related to death at 36 months (chi2 value=7.3, p=0.026), reason for stopping was not (chi2 value=0.57, p=0.45). CONCLUSION: Unlike in non-heart failure populations, dyspnoea as the reason for stopping an exercise test in CHF subjects is not associated with increased mortality. CHF patients should be assessed for treatments such as cardiac resynchronisation therapy by the degree of exercise intolerance, not the nature of their symptoms.

The third heart sound for diagnosis of acute heart failure.

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.

Cardiac asthma in elderly patients: incidence, clinical presentation and outcome.

BACKGROUND: Cardiac asthma is common, but has been poorly investigated. The objective was to compare the characteristics and outcome of cardiac asthma with that of classical congestive heart failure (CHF) in elderly patients. METHODS: Prospective study in an 1,800-bed teaching hospital. RESULTS: Two hundred and twelve consecutive patients aged > or = 65 years presenting with dyspnea due to CHF (mean age of 82 +/- 8 years) were included. Findings of cardiac echocardiography and natriuretic peptides levels were used to confirm CHF. Cardiac asthma patients were defined as a patient with CHF and wheezing reported by attending physician upon admission to the emergency department. The CHF group (n = 137) and the cardiac asthma group (n = 75), differed for tobacco use (34% vs. 59%, p < 0.05), history of chronic obstructive pulmonary disease (16% vs. 47%, p < 0.05), peripheral arterial disease (10% vs. 24%, p < 0.05). Patients with cardiac asthma had a significantly lower pH (7.38 +/- 0.08 vs. 7.43 +/- 0.06, p < 0.05), and a higher PaCO2 (47 +/- 15 vs. 41 +/- 11 mmHg, p < 0.05) at admission. In the cardiac asthma group, patients had greater distal airway obstruction: forced expiratory volume in 1 second of 1.09 vs. 1.33 Liter (p < 0.05), and a forced expiratory flow at 25% to 75% of vital capacity of 0.76 vs. 0.99 Liter (p < 0.05). The in-hospital (23% vs. 19%) and one year mortality (48% vs. 43%) rates were similar. CONCLUSION: Patients with cardiac asthma represented one third of CHF in elderly patients. They were more hypercapnic and experienced more distal airway obstruction. However, outcomes were similar.

Disnea paroxística durante el sueño

La disnea paroxística nocturna o durante el sueño se ha considerado durante muchos años como un síntoma específico de la insuficiencia cardiaca congestiva con fallo ventricular izquierdo y su existencia era además un signo de mal pronóstico. Con los estudios respiratorios durante el sueño se ha podido comprobar que las apneas, sean centrales u obstructivas, juegan un papel fundamental en este trastorno. Asimismo se ha podido demostrar que pacientes con otras enfermedades, como el asma bronquial, la EPOC, las restrictivas pulmonares o las neuro-musculares, tienen las primeras alteraciones respiratorias durante el sueño y por tanto pueden despertarse durante la noche con sensación de falta de aire. Para facilitar su compresión propongo la denominación de "choking" nocturno al despertar brusco con disnea. En el interrogatorio clínico hay que sospechar, en primer lugar, la obstrucción de la vía respiratoria alta que aparece en la apnea obstructiva del sueño, la hipertrofia amigdalar o macroglosia. Otras etiologías son más difíciles de detectar, como la existencia de un reflujo gastro-esofágico durante la noche, crisis de terror, pánico y otras parasomnias (AU)

Airway obstruction and bronchial hyperresponsiveness in left ventricular failure and mitral stenosis.

Small and large airways narrow in LVF and the term cardiac asthma is often used. However, current usage of this term is inconsistent and its meaning is therefore ambiguous. The term is better avoided despite several emerging similarities with bronchial asthma. Airway narrowing may be precipitated by acute elevation of pulmonary or bronchial vascular pressures. This appears to be mainly due to reflex bronchoconstriction. The afferents of this reflex are C-fibers with their endings in the lung parenchyma, bronchi, and pulmonary blood vessels and RAR in the larger airways, and they run in the vagus nerves, as do the efferent bronchoconstrictor fibers. Chronic elevation of pulmonary vascular pressures, as in mitral stenosis, are also associated with airway narrowing. Pulmonary edema (in the absence of vascular hypertension) also causes reflex bronchoconstriction. Bronchial responsiveness to bronchoconstrictor drugs is increased in LVF, partly, at least, due to reflex mechanisms. Bronchial mucosal swelling may also contribute. Narrowing by nonreflex mechanisms definitely occurs and there is direct evidence that decreased lung volume caused by pulmonary edema may cause this. There is little evidence for bronchial narrowing due to the mechanical effect of peribronchial edema, or by swelling of the bronchial mucosa. However, edema foam may terminally cause grave obstruction. Patients with LVF are commonly treated with bronchodilator drugs, but the basis for this approach needs further clarification.

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.

Normal airway responsiveness to methacholine in cardiac asthma.

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.

[Effect of complications in the acute period of myocardial infarction on physical exertion tolerance at the hospital stage of rehabilitation]. / Vliianie oslozhnenii ostrogo perioda infarkta miokarda na perenosimost' fizicheskoi nagruzki na statsionarnom étape reabilitatsii.

Physical stress tolerance and its hemodynamic support were examined in 95 patients with early myocardial infarction, 50 normal subjects and 25 coronary patients. It is suggested that the stress tolerance test is advisable at an early stage of complicated macrofocal myocardial infarction. The safety of the test improves considerably where it is performed under continuous electrocardiographic and chest-rheographic control. An abnormal diastolic impedance wave, emerging during exercise, may serve an additional diagnostic indicator of stress intolerance.

Relation between cardiac dyspnea and left ventricular function. A non-invasive study of 67-year-old men.

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.

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.