How may dyspnea present in heart failure?

A complex respiratory syndrome develops in heart failure, especially in the later stages (Table I). The main symptom is dyspnea, and the main sign is hyperventilation on exertion, followed by the less frequently investigated respiratory dysrhythmias.


Pulmonary hypertension

Restrictive pattern

Decreased pulmonary perfusion

Bronchial hyperactivity

Ventilation-perfusion mismatch

Reduced pulmonary muscle function

Signs and symptoms

Hyperventilation at rest and on exertion

Altered respiratory rhythm and pattern

Effort and rest dyspnea

Table I. Respiratory abnormalities in heart failure.

Effort dyspnea and nocturnal dyspnea can be elicited by direct questioning. As some patients may deny its existence due to their sedentary lifestyle, it is important to ask the patient and partner precise questions as to telltale clues:

Limitations on functional autonomy.

Number of pillows used at night (orthopnea).

Sudden episodes of shortness of breath with no apparent cause on lying flat (paroxysmal nocturnal dyspnea).

Altered sleep pattern, including anxiety, cough, sweating, and/or an altered respiratory rhythm (eg, periodic breathing and nocturnal apnea).

Acute dyspnea. Dyspnea can be sudden and associated with angina (night or day). Severe rest dyspnea associated with bronchospasm is compatible with cardiac asthma; sudden-onset rapidly worsening dyspnea is characteristic of acute pulmonary edema. Other signs and symptoms may be present, such as sibilant breath sounds and cough with whitish sputum (or pink in acute pulmonary edema).

Nocturnal apnea

Patients may complain of insomnia, disturbed sleep (with phases of apnea followed by wakening with hyperpnea), daytime drowsiness with associated tiredness, and sometimes paroxysmal nocturnal dyspnea. The classic expression of the altered ventilation pattern is nocturnal dyspnea, which may be central or obstructive. Apnea and hypopnea are classified as central if the neurologic drive to the respiratory muscles ceases temporarily, and obstructive if respiratory effort increases in response to flow obstruction. In heart failure, nocturnal apnea is usually central. Voluntary control of breathing ceases during sleep, leaving blood gas exchange as the sole determinant of respiratory control. Sympathetic nervous system activation and changes in cardiac loading are the two main pathophysiologic characteristics of nocturnal dyspnea.

Obstructive apnea is characterized by airflow interruption due to decreased tonic input to the upper airways muscles, causing the pharynx to relax and the tongue to fall back over the larynx causing apnea. Respiratory drive increases with the fall in arterial 02 partial pressure and the rise in PCOr The exaggerated negative intrathoracic pressure generated during the inspiratory effort is vigorous but inefficient because it pushes against blocked airways. The heart has to work harder against the extra load caused by this pressure. The increase in pressure gradient between the left ventricle and thorax/pericardium (intra-/extracavity pressure gradient) causes an increase in telesystolic left ventricular pressure (a determinant of afterload). Increased afterload lowers left ventricular releasing velocity. Exaggerated intrathoracic negative pressure causes increased venous return to the right ventricle, right ventricular distension, and paradoxical movement of the interventricular septum to the left, obstructing left ventricular filling. Thus, nocturnal apnea decreases cardiac output and increases left ventricular filling pressures, predisposing to nocturnal myocardial ischemia and pulmonary edema. Hypoxia causes pulmonary vasoconstriction and increased pulmonary pressure, compounding the risk of myocardial ischemia and arrhythmias. Apnea, hypoxia, hypercapnia, reduced cardiac output, and wakening combine to cause sympathetic stimulation that increases neuromuscular activation.

Central apnea

Central apnea associated with Cheyne-Stokes breathing is the form of periodic breathing characterized by a crescendo-decrescendo pattern of vital capacity. Episodes of central apnea alternate with moments of hyperpnea. With the same degree of left ventricular dysfunction, patients with central apnea have a greater incidence of hyperventilation and are more hypocapnic than those without central apnea when either asleep or awake. Pulmonary congestion stimulates the pulmonary juxtacapillary receptors, thus causing hyperventilation. Central apnea occurs when the PC02 falls below the apneic threshold. Mild hypoxia and increased ventilatory response to chemical stimuli during apnea contribute to increasing ventilation and hypocapnia at the end of each episode. The duration of apneic episodes is proportional to the value preceding ventilation and to the degree of hypocapnia. Alternatively, the length of the hyperpneic phase of periodic breathing is proportional to the circulatory delay between the lungs and carotid bodies (expressing delayed recognition of blood gas exchange by the intrapulmonary chemore-ceptors). Circulation time is inversely proportional to cardiac output; hence the length of the hyperpneic phase is a function of the severity of heart failure. Hyperpnea significantly increases intrathoracic negative pressure, and consequently the load on the left ventricle. Central apnea in turn stimulates sympathetic activation, with all its well-documented negative effects. The clinical severity of central apnea can be assessed by the frequency of apneic and hypo-pneic episodes, with a decrease in oxygen saturation in arterial blood (Sa02)and number of awakenings. Patients reporting sleep disturbance have at least 10 to 15 episodes of apnea-hypopnea per hour.

How to differentiate dyspnea (Table II)

Simple observation readily distinguishes obstructive from central apnea. Obstructive apnea, typical of the snorer, is respiratory arrest due to airway obstruction by collapse of the tongue and pharyngeal muscles while the respiratory apparatus continues to work with inefficient inspiratory effort. Central apnea is characterized by a progressive decline in respiration until apnea is reached, when the thoracic cage is immobile. If this occurs while the patient is awake, there is a tendency to fall asleep followed by sudden awakening with hyperpnea. Respiratory periodism is therefore a serious risk when driving.

In any complaint of dyspnea, the history and physical examination will point to a differential diagnosis and/or pulmonary comorbidity. The following help to exclude dyspnea due to bronchial disease or bronchial asthma: absence of heart disease (always present in cardiac dyspnea), mode of onset (slow in bronchial disease), degree of sweating (increased in cardiac dyspnea), response to specific therapy (diuretics in cardiac dyspnea, bron-chodilators in bronchial dyspnea), and chest x-ray (interstitial and alveolar edema in cardiac dyspnea). The shape of the chest and a history of occupational dust exposure or allergic diathesis will point to respiratory disease. Lung function investigations are required in obstruction, computed tomography in suspected interstitial disease or cancer, and perfiision/ventilation scintigraphy and lower-limb venous Doppler in suspected pulmonary embolism. Pallor suggests anemia,

which may be the sole cause of dyspnea if confirmed by revealed by the respiratory pattern and blood gas analy the full blood count. A psychogenic disorder may be sis (a low PC02 suggests hyperventilation).

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