Respiratory pathologies may not always be clear with standard history questions. Additional questions worth asking include:
How long has the dyspnea been present? ( Is this a new problem, or worsening of an existing condition?)
Was the onset gradual or abrupt? (Slow would be more suggestive of something like an infection whereas abrupt might suggest something truly acute like a PE).
Is the SOB made worse in certain positions? (Orthopnea, as we see in heart failure).
Does the patient have a productive cough? Is this a new development? (Chronic bronchitis has a chronic productive cough, whereas Pneumonia and ACPE will have a more acute onset).
Does the patient have chest pain? (...And what does it feel like? Sharp/pinpoint usually means PE, Sharp and diffuse with exacerbation on inspiration suggests pneumonia, and tight, squeezing/pressure/weight suggests ischemia).
Is the patient coughing up blood or discoloured sputum? (Blood suggests things like TB, ACPE, or PE. Discoloured sputum, particularly green or yellow, with a foul smell, suggests infection).
Asthma: Asthma is a reactive airway disease. People with asthma have an exaggerated immune response when environmental irritants, are inhaled, or they are exposed to higher than normal levels of physical or emotional stress. Mast cells in the walls or the bronchioles release inflammatory agents leading to bronchoconstriction. At the same time goblet cells increase the production of mucous to trap the perceived irritants. As a result there is restriction on air in and out of the lungs. The main problem is air trapping, due to the auto-PEEP generated by this condition. The more the asthmatic fights to move air into the lungs, the less they are able to expel. Fortunately this is a reversible condition. Salbutamol may be used to stimulate Beta 2 adrenergic receptors, triggering dilation of the bronchioles. In some services, corticosteroids may be utilized to address the inflammatory response itself. Epinephrine may also be utilized in severe cases. The asthmatic patient will present with varying levels of distress depending upon how bad the acute attack is. Tripoding, is a common physical position, as is the use of accessory muscles to assist in respiration. Cyanosis, and <5 word dyspnea should be concerning. Auscultation will reveal wheezes, or in severe cases a silent chest. Treatment is aimed at opening up constricted airways, and increasing oxygen flow to the alveoli.
COPD:
This is a family of disorders, composed primarily of emphysema and chronic bronchitis. In emphysema, the presence of an aggravating factor, such as cigarette smoking, triggers an inflammatory response. This leads to destruction of the alveolar septa; causing hyperinflated alveoli, air trapping, and increased physiological dead space. In chronic bronchitis, there is the development of an abnormal number and size of goblet cells in the bronchioles. This leads to overproduction of mucous, and plugging of the bronchioles. These illnesses often occur concurrently, and are thus listed under the umbrella term of COPD. These patients are often short of breath, and may have abnormally low oxygen saturation due to chronic retention of CO2. This is normal for these people. COPD exacerbations may occur when the patient has to perform higher than normal physical exertion, spends prolonged time in hot humid environments, or is affected by a respiratory infection. These patients benefit from CPAP as it splints open airways and can be concurrently administered salbutamol.
Pneumonia: When a pathogen enters the lungs it is usually caught by mucous and cilia, and is swept up and out of the airway. In the event that something gets past these defensive structures, alveolar macrophages are present to address the threat. When a pathogen enters the alveoli, macrophages are activated, and engage in phagocytosis. They also release cytokines which trigger an inflammatory response, in order to call in additional immune cells for backup. The downside to this is that the increase in vascular permeability, at the alveolar level, leads to fluid accumulation in the alveoli themselves. This results in a decrease in gas exchange in the lungs. The resulting hypoxia triggers an increase in respiratory rate, an increase in heart rate, and a decrease in oxygen saturation. Assessment will typically reveal a febrile state, crackles upon inspiration, a productive cough, and the patient usually will complain of pleuritic chest pain.
Treatment at the prehospital level involves 3 primary objectives:
Increase oxygenation with supplemental O2 if needed.
Decrease fluid accumulation by giving salbutamol to open up the bronchioles, atrovent in some services, and providing CPAP if they meet the directive. If in doubt patch about the CPAP.
Decrease the fever passively by removing tight/excess clothing.
Pulmonary Embolism: This is a deadly clinical scenario that can lead to rapid patient deterioration and death. The pathophysiology is important to understand because it affects both pulmonary and cardiac systems in critical ways. 95% of PE are the result of an embolus that originates from a DVT in the legs, either the calf or the thigh. This embolus breaks loose and travels to the right side of the heart, from which it passes into pulmonary circulation, and occludes a pulmonary artery. The result is that blood cannot pass the occlusion into the affected lung region. This has a twofold effect. First, it leads to the inability of gas exchange in the affected lung (V:Q mismatch), which causes arterial CO2 levels to rise and arterial O2 levels to drop. This leads to a state of respiratory acidosis. Additionally, an inflammatory process begins at the area of the embolus as an immune response occurs, and cellular necrosis takes place in infarcted tissues. The result is the accumulation of debris and fluid in the bronchioles surrounding the embolus, as well as bronchoconstriction. This obviously further impairs any chance of oxygenation. Second, and possibly even more critically, the embolus causes a back pressure that increases the resistance against which the right ventricle must push in order to perfuse the rest of the lung tissues. The resulting back pressure leads to a decrease in SV from the right ventricle, and ultimately a decrease in cardiac output. The heart's only compensatory mechanism for this is to increase rate, leading to tachycardia. The body also attempts systemic vasoconstriction in order to increase SVR, to try and provide more preload to the right side of the heart. Unfortunately this is futile because no amount of increase preload is going to overcome the increasing back pressure caused by the embolus.
Recognizing a PE:
Look for signs of a DVT. Also ask about recent periods of prolonged immobility, recent travel, or recent surgeries.
RULE OUT STEMI. Gieven the overlap of symptoms, it is better to be safe and do a 12 lead.
Look for a LOW etco2 reading. The inability to exchange arterial CO2 means that expired CO2 levels will be quite low. In general they will be 25mmHg or less.
Common symptoms of PE:
Tachycardia
Dyspnea
Pleuritic/sharp, often pinpoint, chest pain
Hypotension
Low ETCO2, Low SPO2
Signs of DVT or Hx suggestive of one.
Risk Factors for DVT:
Recent surgery
Pregnancy
Varicose veins
Recent fracture
Prolonged immobility
Treatment: There are 2 main goals with treatment:
Improve Oxygenation with supplemental O2. NOTE: STAY AWAY FROM CPAP. CPAP increases intrathoracic pressure on the vena cava, which can risk dropping preload to the heart. This can be fatal to PE patients.
Manage cardiac output by treating hypotension with fluids.
***NO MATTER WHAT, DO NOT GIVE NITROGLYCERINE TO A PE PATIENT!!!!! This is going to drop preload and could ultimately result in cardiac arrest.
Pneumothorax: This is a collection of air within the pleural space, leading to gradual collapse of the affected lung. In a spontaneous pneumothorax, a weak area, or bleb, ruptures. This allows air to escape the alveoli into the intrapleural space. Normally this space has a negative pressure, allowing the lungs to expand with breathing. However, this trapped air experts a positive pressure, impeding lung expansion. The result is hypoventilation and decrease in tidal volume. A spontaneous pneumothorax can progress to a tension pneumothorax if additional air is allowed to enter this space. This gradually compresses the lung further until ventilation is no longer possible. These patients present with:
Sudden sharp, pleuritic, chest pain on the affected side.
Severe dyspnea and tachypnea
Unilateral breath sounds
Narrowing pulse pressure
Hypotension if the pneumothorax causes a mediastinal shift and compresses the vena cava.
Tachycardia
Low SPO2
Alterations in LOA
Risk factors include: Smoking, COPD/Asthma, and tall slender stature.
Treatment includes:
Recognition of symptoms.
Improving oxygenation
Managing hypotension
Needle decompression if ALS is available.
Top 5 Killer Differentials for Shortness of breath (A.C.I.D.S.)
ACPE
COPD/Asthma
Infarction (MI or PE)
DKA/Metabolic acidosis
Sepsis/Pneumona
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