APPROACH TO
DYSPNEA
IM 1.10
DYSPNOEA
subjective experience of breathing discomfort that consists
of qualitatively distinct sensations that vary in intensity.
The experience derives from interactions among multiple
physiological, psychological,social, and environmental
factors
PATIENTS PERCEPTIONS
Unsatisfied inspiration
Chest tightness
Sensation of feeling breathless
Cannot get enough air
Hunger for air
Incomplete exhalation
PATHOPHYSIOLOGY
:
Respiratory diseases can stimulate breathing and dyspnea by:
Stimulating intrapulmonary sensory nerves (e.g. Pneumothorax,
interstitial inflammation and pulmonary embolus)
Increasing the mechanical load on the respiratory muscles (e.g. airflow
obstruction or pulmonary fibrosis)
Causing hypoxia, hypercapnia or acidosis, stimulating chemoreceptors.
Cardiac failure can stimulate breathing and dyspnea by:
pulmonary congestion reduces lung compliance and can also
obstruct the small airways.
During exercise, reduced cardiac output limits oxygen supply to
the skeletal muscles, causing early lactic acidemia and further
stimulating breathing via the central chemoreceptors.
COMMON PULMONARY CAUSES
Obstructive lung disease
Asthma/COPD (Chronic Bronchitis, Emphysema)
Pneumonia
Pulmonary embolism
Pneumothorax
COMMON CARDIAC CAUSES
Acute coronary syndromes
CHF
Arrhythmias
Valvular heart disease
SIGNALING PATHWAYS UNDERLYING DYSPNEA
TYPES OF DYSPNEA
EXERTIONAL DYSPNEA- Dyspnea due to exercise
ORTHOPNEA - Shortness of breath that occurs while lying flat and is
relieved by sitting or standing. (CHF, pregnancy, respiratory muscle
weakness)
PAROXYSMAL NOCTURNAL DYSPNEA -Acute shortness of breath almost always
accompanied by coughing and wheezing. This respiratory distress usually occurs
when a person is already sleep in a reclining position (HEART FAILURE-early
night, ASTHMA-late night)
RESTING DYSPNEA- Dyspnea at rest
ORTHOPNEA
Dyspnea that occurs in the recumbent position
Redistribution of fluid from the abdomen and lower body into the
chest
Increased work of breathing due to decreased lung compliance,
In patients with ascites or hepatomegaly, elevation of the diaphragm.
Orthopnea typically occurs in the awake patient within 1–2 min of
lying down and may be relieved by raising the head and chest with
pillows or an adjustable bed.
With more severe HF, patients may end up sleeping in a recliner
chair or sitting up
For some, orthopnea may diminish as symptoms of right HF appear
Nocturnal cough related to pulmonary congestion
PAROXYSMAL NOCTURNAL
DYSPNEA
Episodes of shortness of breath that awaken a patient suddenly from
sleep
Anxiety and suffocation
Sitting upright for relief
In contrast to orthopnea, PND usually occurs after prolonged
recumbency
Less predictable in occurrence
May require 30 min or longer in the upright position for relief
• Coughing and wheezing due to increased bronchial arterial pressure
leading to airway compression and interstitial pulmonary edema
causing increased airway resistance.
• Acute pulmonary edema, due to marked elevation of the pulmonary
capillary wedge pressure, is manifested by severe shortness of breath
and pink, frothy sputum
Cheyne-Stokes respiration and central sleep apnea may precipitate
episodes of PND in HF and are related to increased sensitivity of the
respiratory center to arterial PCO2 and a prolonged circulatory time
Obstructive sleep apnea,can be treated with positive airway
pressure therapy
Central sleep apnea has no proven therapy beyond the directed
treatment of HF
DIFERENTIAL DIAGNOSIS
APPROACH TO DYSPNEA
History
Physical examination
Chest imaging
Lab.studies
HISTORY
The patient should be asked to describe in his own words:
what the discomfort feels like as well as the effect of
position,infections and environmental stimuli on the
dyspnea.
Onset,duration and frequency
Precipitating factors
Relieving factors
Associated symptoms
EXAMPLES
Chest tightness might suggest the possibility of
bronchoconstriction
Sensation of inability to take a deep breath may
correlate with dynamic hyperinflation from COPD.
Orthopnea is a common indicator of congestive heart failure (CHF)
Mechanical impairment of the diaphragm associated with obesity
Asthma triggered by esophageal reflux.
Nocturnal dyspnea suggests CHF or asthma.
Acute, intermittent episodes of dyspnea are more likely to reflect
episodes of myocardial ischemia, bronchospasm, or pulmonary
embolism
• Chronic persistent dyspnea is more typical of COPD, interstitial lung
disease, and chronic thromboembolic disease
• Information on risk factors for drug-induced or occupational lung
disease and for coronary artery disease should be elicited
PHYSICAL EXAMINATION
Vital signs
presence of fever might point toward an underlying
infectious or inflammatory process
presence of tachycardia might be associated with many
different underlying processes including fever, cardiac
dysfunction
presence of resting hypoxemia suggests processes
involving hypercapnia, ventilation-perfusion mismatch,
shunt, or impairment in diffusion capacity
Exertional oxygen saturation
Presence of hypertension in the setting of a heart failure
might point toward diastolic dysfunction
■ Whether the patient is able to complete full sentences while talking.
■ Use of accessory muscles of respirations
■ paradoxical breathing or sitting in tripod position
■ Signs of pallor, cyanosis, clubbing and pedal oedema are looked
■ Haemodynamic stability
■ whether the patient is able to maintain saturation on room air is
assessed using pulse oximetry.
Measuring blood pressure pulsus paradoxus should be
watched for as its presence points to pericardial disease,
restrictive heart disease.
The symmetry of chest wall movements with respiration is
observed
Percussion (e.g., dull note in pleural effusion, hyper resonant
in tension pneumothorax).
Auscultation (wheezes, rhonchi, prolonged expiratory phase,
and diminished breath sounds are clues to disorders of the
airways; rales suggest interstitial edema or fibrosis)
The cardiac examination should focus on
Signs of elevated right heart pressures (jugular venous
distention, edema, accentuated pulmonic component
to the second heart sound)
Left ventricular dysfunction (S3and S4 gallops)
Valvular disease (murmurs).
On abdominal examination
paradoxical movement of the abdomen
increased respiratory distress in the supine position
inward motion during inspiration is a sign of diaphragmatic
Weakness
rounding of the abdomen during exhalation is suggestive of
pulmonary edema.
CHEST EXAMINATION
Lung volumes
Hyperinflation - obstructive lung disease
Low lung volumes -interstitial edema or fibrosis,
diaphragmatic dysfunction, or impaired chest wall
motion
The pulmonary parenchyma should be examined for
evidence of interstitial disease, infiltrates, and
emphysema.
Prominent pulmonary vasculature in the upper zones-
pulmonary venous hypertension
enlarged central pulmonary arteries - pulmonary arterial
hypertension.
An enlarged cardiac silhouette -dilated cardiomyopathy or
valvular disease.
Bilateral pleural effusions are typical of CHF and some forms
of collagen-vascular disease.
Unilateral effusions -carcinoma and pulmonary embolism but
may also occur in heart failure or in the case of a
parapneumonic effusion.
CT of the chest is generally reserved for further
evaluation of the lung parenchyma (interstitial lung disease)
and possible pulmonary embolism if there is diagnostic
uncertainty.
LABOROTARY
INVESTIGATIONS
Hematocrit
metabolic panel (an elevated bicarbonate might point
toward the possibility of carbon dioxide retention that might
be seen in chronic respiratory failure)
Arterial blood gas (ABG) analysis will help in knowing the type of
respiratory failure and also gives information about the acid-base
state of the patient
Electrocardiography –ventricular hypertrophy and prior myocardial
infarction
Spirometry-obstructive ventilatory defect and suggest the
possibility of a restrictive ventilatory defect
Echocardiography -systolic dysfunction, pulmonary hypertension,
valvular heart disease
Bronchoprovocation testing may be useful in patients with
intermittent symptoms suggestive of asthma who have a normal
physical examination and spirometry
Measurement of brain natriuretic peptide levels in serum is
increasingly used to assess for CHF in patients presenting with acute
dyspnea
DISTINGUISHING CARDIOVASCULAR
FROM RESPIRATORY SYSTEM DYSPNEA
Cardiopulmonary exercise test (CPET)
• If, at peak exercise, the patient achieves predicted maximal
ventilation, demonstrates an increase in dead space or
hypoxemia, or develops bronchospasm, the respiratory system
may be the cause of the problem
• Alternatively if the heart rate is >85% of the predicted
maximum, if the blood pressure becomes excessively high or
decreases ,if the O2 pulse (O2 consumption/heart rate, an
indicator of stroke volume) falls, or if there are ischemic changes
on the electrocardiogram,an abnormality of the cardiovascular
system is likely the explanation for the breathing discomfort.
TREATMENT
The first goal is to correct the underlying conditions driving dyspnea
Multiple different interventions- multifactorial causes
Supplemental O2 should be administered if the resting O2 saturation is
≤88% or if the patient’s saturation drops to these levels with activity or
sleep
Opioids have been shown to reduce symptoms of dyspnea, largely
through reducing air hunger, thus likely suppressing respiratory drive and
influencing cortical activity
THANK YOU
