What is dyspnea? Dyspnea is the perception of an inability to breathe comfortably. It may or may not correspond with hypoxemia. An acutely dyspneic patient is often highly challenging as a physician must rapidly work through several possible differential diagnoses while managing a potentially life-threatening situation.
Acute dyspnea is generally caused by one of five processes:
1. Hypoxemia
2. Hypercapnea
3. Acidemia
4. Poor oxygen delivery to peripheral tissues without hypoxemia
5. Miscellaneous
Hypoxemia
This is what people most commonly consider when thinking of a dyspneic patient. Potential etiologies resulting in hypoxemic dyspnea include:
Pulmonary Edema (Both Cardiogenic and noncardiogenic)
Pneumonia
Pulmonary Embolism
Pleural Effusion
COPD Exacerbation
Less common etiologies include ILD, Pneumothorax, Mucus Plug, or Atelectasis.
Hypercarbia
This is NOT a list of all the things that cause hypercapneic respiratory failure! Remember that many things that lead to hypercarbia do NOT present with dyspnea; instead, they can present with somnolence, bradypnea, etc.
Hypercarbic dyspnea can be caused by:
COPD Exacerbation
Asthma Exacerbation
Acute neuro/neuromusclar disease (i.e MG, Transverse myelitis, GBS)
Herein, we propose a method for working through an acutely dyspneic patient.
Acidemia
Acidemia (besides that caused by hypercapnia) can cause dyspnea. The most likely to cause dyspnea are ketoacidosis and lactic acidosis.
Poor Oxygen Deliver to Peripheral Tissues
Shock (without hypoxemia) can result in dyspnea. This includes:
Anemia
Low output heart failure
Obstructive shock (i.e. Massive PE, tamponade, or a tension pneumothorax).
Miscellaneous
Other causes include:
ACS
Upper Airway obstruction (including a foreign body, angioedema, abscesses or other infections, anaphylaxis, or airway trauma)
Anxiety or Panic Attack
Acute Pain
End of Life Dyspnea
What approach do I take in managing an acutely dyspneic patient?
1. Your first priority in the acutely dyspneic patient is managing ABCs.
A = Airway
How to assess:
Check for breath sounds (auscultating or just counting)
Listen to patient’s voice if they are able to talk
Call anesthesia (i.e. CALL A CODE) if you think intubation on the floor is needed. You can call the ICU fellow if you think patient MAY need to be intubated in the near future and this could happen in the ICU. Always err on the side of calling a code if you are concerned.
While you are waiting for additional people to arrive:
Position the airway to improve airflow
Utilize an airway adjunct if necessary
There are two methods of positioning the airway (click on the link to watch a video demonstrating both methods).
One is the Head-Tilt Chin-Lift: in this method, you apply downward pressure to the patient's forehead with one hand while the tips of your index & middle fingers should lift the mandible at the chin. This moves the tongue from the posterior pharynx.
The second method is the Jaw Thrust. Place the heels of both hands on the parieto-occipital areas on each side of the patient's head and grasp the angles of the mandible with the index and long fingers. Displace the jaw anteriorly.
Airway adjuncts are also helpful but they should ONLY BE USED BY EXPERIENCED PROVIDERS. Make sure you are comfortable using an airway adjunct before attempting one during a rapid response or code.
Two options for airway adjucts include the oropharyngeal airway or nasopharyngeal airway. (Again, click the links if you'd like to see videos of the management of these airways).
An oropharyngeal airway should be used only in a patient who is deeply unresponsive and not maintaining their airway (i.e. someone you could intubate in their present condition). You can cause vomiting and aspiration if the patient is too awake.
Nasophayngeal airways come in different sizes based on internal diameter. You coat the airway with water-soluble lubricant or anesthetic jelly and insert along floor of naris into posterior pharynx behind tongue. Be careful when sizing; a too long airway will actually go into esophagus and cause you to ventilate the stomach. These also cause nasal bleeding in ~30% of patients and can lead to aspiration of blood.
B = Breathing
How to assess:
Count out your respiratory rate
Look at chest wall movement
Auscultate
Check Pulse Ox
You can apply oxygen if respirations are adequate but sats are low. Consider initiating BiPAP right away on floor (requires ICU transfer) to help work of breathing if patient A&O x 4.
Bag Mask Ventilate if ineffective respirations or no respirations! Call a code if you are doing this.
C = Circulation
How to assess:
Palpate pulses
Auscultate heart
Check blood pressure
Consider EKG or Tele
Check skin color and capillary refill time
Use the principles from the Hypotension RRT lecture to help guide you!
2. Start with a focused evaluation: get a Chest X-ray and do a concentrated cardiac, pulmonary, and extremity exam while you are waiting for the X-ray.
Having just these pieces can clue you in to one of several illness scripts for the acutely dyspneic patient:
1. Focal Crackles and Focal Opacity on CXR = Pneumonia
Other supporting data for pneumonia includes hypoxia, the presence of any SIRS criteria (tachycardia, tachypnea, fever, leukocytosis), cough +/- sputum production, elevated procalcitonin, and a recent URI.
Consider ordering blood and sputum cultures and starting antibiotic therapy.
2. Diffuse Coarse Crackles and Diffuse Alveolar Opacities on CXR = Pulmonary Edema
Other supporting data include a history of CHF, MI, or CAD; the presence of PND, orthopnea, or DOE; S3, JVD, rales, any cardiac murmur, and/or leg edema on examination.
Consider:
Cardiogenic versus non-cardiogenic? (TRALI, TACO, ARDS, etc.)
IV diuretic therapy
Telemetry
Labs & EKG (BNP, troponins, BMP)
BiPAP
3. Unilateral decreased breath sounds + pleural effusion on CXR = Pleural Effusion.
Other supporting data include the presence of dullness to percussion and asymmetric chest expansion. The absence of reduced tactile fremitus makes a pleural effusion less likely.
Consider a thoracentesis as we;; as further workup for underlying cause & treatment of that etiology (i.e. diuretics for CHF).
4. Unilateral decreased breath sounds + pneumothorax on CXR = Pneumothorax
In general, management depends on the size, degree of clinical compromise, and if it is a primary or secondary PTX. However, if this is making your patient is dyspneic, you need to intervene.Start with high-flow supplemental oxygen & monitor response. If tension pneumothorax (i.e. coding), add in emergent needle thoracostomy & call CT surgery STAT.
5. Globally decreased breath sounds +/- wheezes + CXR without opacities = COPD or Asthma.
Supportive data would include a history of smoking, COPD/asthma, or wheezing as well as history of recent viral URI.
COPD management pearls include:
Oxygen for sats <88%
STAT albuterol + ipratroprium
Strongly consider systemic steroids: oral prednisone versus IV methylprednisone if seriously ill
Consider BiPAP; page ICU.
Azithromycin is added if patient meets one of the following: Increased dyspnea, sputum volume and purulence; increased sputum purulence with either increased dyspnea OR sputum volume; need for mechanical ventilation.
Asthma management pearls include:
Oxygen for saturations <90%
STAT albuterol: consider continuous versus MDI versus standard neb
Consider steroids: oral prednisone versus IV methylprednisone if seriously ill
ICU consult if not improving with these therapies or if giving IV steroids
6. Normal lung exam and normal CXR: PE?
You should strongly consider evaluating for PE in any acutely dyspneic patient with a normal lung exam and normal CXR. Use any of these clinical prediction rules to evaluate. Well's criteria and the Geneva Revised Score are helpful.
Consider the following in this patient:
STAT CT PE
Heparin drip
ICU transfer +/- TPA for massive PE (TPA is not well-validated in PE: don’t be afraid to call ICU fellow first!).
You can use PESI score for help with risk stratification or sPESI.
My patient is low risk based on that score and doesn't fit any other illness script… where do I go from here?
1. Review your patient's oxygen saturation!
Notice this is the first time we’ve discussed oxygen sats! It’s important to note that respiratory distress is NOT defined by hypoxemia and hypoxemia is NOT required for any of these diagnoses.
If O2 sats are low, grab an ABG. (You should have hopefully already started them on oxygen back in the ABCs)
2. What to do with the patient with a normal CXR, normal exam, and normal sats on room air?
Consider CBC, BMP, ABG/VBG, EKG, d-dimer, troponin based on patient’s history
EKG + trop if you are at all worried about this being an anginal equivalent
Pulsus paradoxus: quick check and can clue you in to a pericardial effusion missed on the CXR
Always consider the life-threatening diagnoses, including ACS, tamponade, PTX, and PE. (It is better to over-test than under, especially early in residency)
Acute onset (minutes to seconds) with chest pain: think PE, ACS, Pneumothorax, or Tachyarrhythmia → pulmonary edema
Look at the Respiratory Pattern? Rapid and unusually shallow = COPD, asthma, anxiety whereas unusually deep (i.e Kussmaul) = metabolic acidosis
References
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