Approach to dyspnea: Clinical sciences
Introduction0:00–0:32
Acute dyspnea is the sensation of difficult or uncomfortable breathing that develops over hours to days. Dyspnea is a common symptom with a wide range of causes including respiratory, cardiovascular, metabolic, neuromuscular, and neurologic conditions.
When approaching a patient with dyspnea, first you should perform an ABCDE assessment, to determine if your patient is unstable or stable.
Unstable0:32–2:33
If they are unstable, first check for alarm signs and symptoms! Check for upper airway obstruction by auscultating for stridor, a high-pitched breathing sound, and by directly examining the airway for oropharyngeal swelling or the presence of a foreign body.
If the airway is clear, evaluate the patient’s breathing by assessing respiratory rate and oxygen saturation. A respiratory rate less than 10 or greater than 20 breaths per minute, or oxygen saturation less than 90% requires acute management.
You should also look for red flag features that signal impending respiratory failure such as confusion, inability to speak in complete sentences, and the use of accessory respiratory muscles, such as the scalenes and intercostals.
In this case, stabilize the airway, breathing, and circulation, which may require removing any airway obstruction, endotracheal intubation and mechanical ventilation.
Some patients might require supplemental oxygen only, but, in both cases, don’t forget to obtain IV access and put your patient on continuous vital sign monitoring.
Now, here’s a high-yield fact to keep in mind! Causes of acute airway obstruction, that might present with stridor, include anaphylaxis, epiglottitis, and the presence of a foreign body.
Suspect anaphylaxis if the patient reports exposure to a known allergen, such as an insect sting, and presents with urticaria, stridor, or wheezing.
On the other hand, epiglottitis most commonly presents with hoarseness and dysphagia in the setting of upper respiratory infection caused by Haemophilus influenzae, as well as Streptococcal and Staphylococcal species.
Now that unstable patients are taken care of, let’s go back to the ABCDE assessment and take a look at stable patients. If your patient is stable, proceed with a focused history and physical examination, and order labs including CBC, BMP, BNP, D-dimer, and cardiac enzymes.
Stable2:33–3:05
Additionally, order imaging, like a chest x-ray, and possibly point of care ultrasound, or POCUS for short. You’ll also want to get an ECG on all patients with dyspnea.First, let's discuss the primary respiratory causes of acute dyspnea, which include pneumothorax, pneumonia, asthma, and COPD exacerbation.
Respiratory causes3:05–3:19
Let’s look at pneumothorax,Consider pneumothorax in a patient with acute dyspnea that reports pleuritic chest pain. On physical exam, decreased breath sounds and hyperresonance to percussion on the affected side are consistent with pneumothorax.
Pneumothorax3:19–4:00
Chest x-ray will show a distinct visceral pleural edge with an absence of distal lung markings, and, in the case of a tension pneumothorax, may show tracheal deviation and mediastinal shift away from the side of the collapsed lung.
POCUS will show absent lung sliding. Keep in mind that patients with tension pneumothorax are usually unstable, so you should skip imaging and perform immediate needle decompression.Another primary respiratory cause of acute dyspnea is pneumonia.
Pneumonia4:00–4:32
A person with pneumonia might report pleuritic chest pain, productive cough, and fever. Their labs will show leukocytosis with left shift, while chest x-ray could show lobar consolidation or diffuse infiltrates.
Common POCUS findings include subpleural consolidation, liver-like echogenicity of the lung, and dynamic air bronchograms.
Asthma and COPD4:32–5:13
Bronchoconstriction during an asthma or COPD exacerbation can cause wheezing, diminished air entry, and a prolonged expiratory phase on physical exam.
Chest x-ray may show lung hyperinflation and flattened diaphragms. History can help distinguish between asthma and COPD.
Individuals with COPD tend to be older, often have a productive cough that worsens over time, and have a history of smoking.Next, let’s move on to cardiovascular causes of acute dyspnea, which include cardiac tamponade, pulmonary embolism, myocardial infarction, arrhythmia, and decompensated heart failure.Let’s start with cardiac tamponade.
Cardiovascular causes5:13–5:28
In these individuals, history finding typically includes chest pain, and the physical findings include pulsus paradoxus and Beck triad, which is hypotension, jugular venous distention, and muffled heart sounds.ECG often shows sinus tachycardia with low voltage QRS complexes or electrical alternans.
Cardiac tamponade5:28–6:12
Chest X-ray might reveal a widened mediastinum and a water bottle sign, where the cardiac silhouette appears enlarged and stretched.
Diagnosis of cardiac tamponade can be confirmed via POCUS or transthoracic echocardiogram or TTE, which typically shows pericardial effusion, as well as diastolic collapse of the right atrium and ventricle.Next up is pulmonary embolism.
Suspect pulmonary embolism in patients with pleuritic chest pain and hemoptysis that have a history of deep vein thrombosis or DVT.
Pulmonary embolism6:12–7:04
Chest x-ray is usually normal. On the other hand, ECG often shows sinus tachycardia, and less frequently the S1Q3T3 pattern, where there’s a large S wave in lead I, and a Q wave and inverted T wave in lead III.
Since massive PE causes strain to the right heart, labs may show elevated cardiac enzymes. The likelihood of PE can be determined by the Wells criteria.
A high-probability Wells score or an intermediate score plus elevated D-dimer should prompt you to order CT pulmonary angiography or CTPA.If the CTPA reveals a filling defect in a pulmonary artery, the diagnosis of pulmonary embolism is confirmed.Another important cardiac cause of acute dyspnea is myocardial infarction.
Suspect myocardial infarction in a person with risk factors for cardiovascular disease who presents with anginal chest pain and diaphoresis.
Myocardial Infarction7:04–7:38
ECG might reveal ST segment elevations or depressions, T wave inversions, and new onset left bundle branch block, while labs will usually show elevated cardiac enzymes from myocardial damage.
All of these findings are suggestive of myocardial infarction!Next, let’s look at arrhythmia.Next, let’s suppose a dyspneic patient presents with palpitations or syncope.
Arrhythmia7:38–8:12
In this case, consider arrhythmia as the cause of their symptoms. On exam, you may detect bradycardia, tachycardia, or an irregular pulse.
The ECG may show a bradyarrhythmia, like heart block, or tachyarrhythmia like atrial fibrillation with rapid ventricular response.
On the other hand, if the cardiac rate and rhythm are normal, consider a paroxysmal arrhythmia, and start cardiac rhythm monitoring to catch the next episode.
Finally, let's not forget acute decompensated heart failure that leads to pulmonary edema. This occurs because the heart isn’t pumping blood efficiently, so it backs up into the pulmonary vein and capillaries.
Acute decompensated heart failure8:12–9:39
As the pressure increases, fluid is leaked from the pulmonary capillaries into the alveoli, leading to pulmonary edema. These individuals may also complain of chest discomfort and orthopnea.
Physical exam will typically reveal jugular venous distention or JVD, rales, and lower limb swelling with pitting edema, while labs usually show an elevated BNP.Chest x-ray often reveals pulmonary edema or even pleural effusion.
In this case order TTE to detect ventricular dysfunction, which supports the diagnosis of acute decompensated heart failure.
Here’s a high yield fact! Not all pulmonary edema is caused by heart failure.
So in those cases, you won’t see ventricular dysfunction on TTE. Some important causes include acute respiratory distress syndrome or ARDS and severe renal failure.
ARDS is characterized by increased permeability of the pulmonary capillaries due to severe inflammation, which can be triggered by conditions like sepsis, pancreatitis, or aspiration.
On the other hand, patients with severe renal failure have impaired excretion of water and solutes, which in turn leads to hypervolemia or fluid overload.Ok, If both respiratory and cardiogenic causes are unlikely, consider metabolic acidosis.
This is because, when there’s build up of acid from excess creation or inability to excrete, the body's reaction is to stimulate the respiratory center in the brainstem; as a result, patients develop hyperventilation to compensate for the acidosis by getting rid of more CO2, which is also an acid.
Metabolic acidosis9:39–10:23
Now, metabolic acidosis can have multiple causes, such as excessive alcohol intake or starvation, while two causes that you need to keep in mind first are diabetic ketoacidosis and salicylate toxicity.
First, let’s start with diabetic ketoacidosis or DKA for short. DKA can trigger compensatory hyperventilation, and cause shortness of breath.
Suspect DKA in a person with a history of diabetes mellitus or DM, who complains of polyuria and polydipsia. On exam, they may show signs of dehydration like dry mucous membranes and poor skin turgor, and have a fruity odor to the breath.
DKA10:23–10:58
Labs will show hyperglycemia, ketonemia, and metabolic acidosis with an elevated anion gap, and ABG will confirm metabolic acidosis and thus confirm the diagnosis of diabetic ketoacidosis.Next, let’s look at salicylate toxicity.
Salicylate toxicity is another metabolic disturbance that can present with acute respiratory symptoms. People who ingest toxic levels of salicylates develop tachypnea due to increased respiratory drive.
Salicylate toxicity10:58–11:42
These individuals often report salicylate ingestion and present with tachypnea. When evaluating a patient with suspected salicylate toxicity, labs will show metabolic acidosis with an elevated anion gap.
Next, check an ABG and serum salicylate level. The presence of metabolic acidosis with respiratory alkalosis is commonly observed in salicylate toxicity, while an elevated serum salicylate level confirms the diagnosis.
Finally, let’s take a look at neuromuscular and neurogenic causes of acute dyspnea. [video editor: dmt transition (16.dtm-dyspnea -> 17.dmt-dyspnea)]First, let’s look at neuromuscular disease.Neuromuscular conditions, like myasthenia gravis and Guillain Barre syndrome, are uncommon but important causes of respiratory distress to consider, particularly if the patient reports a history of neuromuscular disease, or displays signs of neurologic dysfunction like muscle weakness, dysarthria, dysphagia, or ineffective cough.
Neuromuscular/neurogenic causes11:42–11:50
Neuromuscular disease11:50–12:23
Checking an ABG will typically reveal respiratory acidosis in patients with dyspnea due to neuromuscular disease. Lastly, let’s look at acute anxiety and panic disorder.Acute anxiety and panic disorder are psychiatric causes of acute dyspnea that may present during an anxiety-provoking event, such as witnessing an accident, or in the absence of an obvious stressor, like during a panic attack.
Acute anxiety/ panic disorder12:23–13:04
However, this is a diagnosis of exclusion that should be considered only after other more life-threatening causes have been ruled out.
An individual with dyspnea due to anxiety may report associated symptoms of chest tightness, palpitations, and sweating.
Laboratory tests and imaging will be negative for other causes of dyspnea. Using a validated metric, like the 7-question General Anxiety Disorder, or GAD-7 questionnaire can help you confirm the diagnosis.
Alright, as a quick recap… Acute dyspnea is a common symptom in a variety of respiratory, cardiovascular, metabolic, neuromuscular, and neurologic problems, many of which are life-threatening.
Review13:04–14:06
Next consider respiratory conditions including pneumothorax, pneumonia, as well as asthma and COPD exacerbations. Next, evaluate for cardiovascular causes of dyspnea, such as cardiac tamponade, pulmonary embolism, myocardial infarction, arrhythmia, and acute decompensated heart failure with pulmonary edema.
If respiratory and cardiovascular causes have been ruled out, think of causes of metabolic acidosis, such as excessive alcohol intake or starvation, as well as diabetic ketoacidosis and salicylate toxicity.
And finally, consider neuromuscular and neurogenic problems including neuromuscular disease and acute anxiety. of metabolic acidosis such as excessive alcohol intake or starvation as well as diabetic ketoacidosis and salicylate toxicity And finally consider neuromuscular and neurogenic problems including neuromuscular disease and
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