Compare conditions

Put any two — or three — conditions side by side, adult or pediatric, to spot the look-alike differences fast, row by row.

Asthma Exacerbation

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In one line

·The airways clamp shut (smooth muscle spasm), swell up (inflammation led by IgE, mast cells, eosinophils, and leukotrienes), and fill with thick sticky mucus—air cannot get through.

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Normal physiology

·Airways branch from the trachea (windpipe) into smaller and smaller tubes—bronchi, then bronchioles—all the way down to the alveoli (tiny air sacs where oxygen jumps into the blood and carbon dioxide jumps out). Each airway has three layers: a thin inner lining (mucosa) that makes a small amount of mucus to trap dust, a middle layer of smooth muscle that can squeeze or relax to adjust airflow, and mucus glands that keep the lining moist. In a healthy lung, air glides in and out freely, and the immune system stays quiet unless a real germ shows up.

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What goes wrong

·The immune system treats a harmless thing—pollen, cold air, a virus—like a dangerous invader. Mast cells (immune guard cells living in the airway lining) are coated with IgE antibodies (sticky proteins that remember past triggers). When the trigger arrives, mast cells pop open and dump histamine and leukotrienes (chemicals that cause swelling and muscle spasm). The smooth muscle ring around the airway squeezes tight (bronchospasm—like a fist closing around a straw). Eosinophils (white blood cells that normally fight worms) flood into the airway wall and pour out more chemicals that make the lining swell and stay inflamed. Mucus glands kick into overdrive and fill the tube with thick sticky gunk. The airway gets narrow three ways at once: muscle spasm, swelling, and mucus plugs.

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Hallmark signs

·Wheeze (mostly when breathing out)
·Cough (often at night or after exercise)
·Chest tightness or pressure
·Shortness of breath (hard to get enough air)
·Prolonged breathing-out phase (takes longer to exhale)
·Using neck, shoulder, and rib muscles to breathe
·Speaking only a few words at a time or one word per breath
·Silent chest (no wheeze, almost no breath sounds)

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Red flags · escalate now

·Silent chest, speaking only one word at a time, blue skin, or confusion—life-threatening asthma; breathing may stop within minutes
·Carbon dioxide level holding steady or rising during a severe attack—the breathing muscles are exhausting and the lungs are starting to fail
·Little or no improvement after one hour of strong inhaled medicine and steroids—the attack is not responding to standard treatment
·History of being put on a breathing machine for asthma before, or any hospital admission for asthma in the past year—marks the person as high-risk for another severe attack
·Cannot lie flat or can only say one word per breath—the airways are severely blocked

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Workup

·Peak expiratory flow (PEF) or forced expiratory volume in 1 second (FEV₁)
·Pulse oximetry (SpO₂)
·Arterial blood gas (ABG)
·Chest X-ray
·Serum electrolytes (sodium, potassium, magnesium) and glucose
·Complete blood count (CBC)

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Treatment

·Supplemental oxygen by nasal cannula or mask to keep SpO₂ at least 90%, targeting 93–95%
·Short-acting beta-agonist—albuterol (salbutamol)—by nebulizer or metered-dose inhaler with spacer: 4–8 puffs every 20 minutes for the first hour, then every 3–4 hours; or continuous nebulization if the flare-up (exacerbation) is severe
·Ipratropium bromide (a short-acting anticholinergic) added to albuterol in moderate to severe exacerbations
·Systemic corticosteroids: prednisone or prednisolone 40–50 mg by mouth, or methylprednisolone 60–125 mg intravenously if the patient cannot swallow or is vomiting
·Intravenous magnesium sulfate 2 grams infused over 20 minutes for severe exacerbations not responding to initial therapy (PEF or FEV₁ less than 40 percent predicted after 1 hour of maximum treatment)
·Noninvasive positive-pressure ventilation (BiPAP) or endotracheal intubation with mechanical ventilation for impending or actual respiratory failure (rising CO₂, exhaustion, altered mental status, or cardiac arrest)
·Discharge the patient on a 5- to 7-day course of oral corticosteroids (prednisone 40–50 mg daily for adults, 1–2 mg per kilogram daily up to 40 mg for children) and make sure daily controller therapy—an inhaled corticosteroid with or without a long-acting beta-agonist—is started or stepped up

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NCLEX trap

·Non-selective beta blockers (like propranolol) block beta-2 receptors in the airways — those tiny switches help keep the airways open. Blocking them makes the airways squeeze shut even tighter. The fast heart rate happens because the rescue inhaler (albuterol) speeds up the heart AND because low oxygen makes the heart pump harder to deliver what little oxygen is left. The heart rate will come down on its own once the asthma attack is treated and oxygen levels rise.
·In a severe asthma attack, the patient should be breathing SO fast that CO₂ is blown off — so you expect a LOW CO₂. If CO₂ is normal or rising, it means the patient is too tired to push air out anymore. The breathing muscles are giving up. This is a red-alert sign that the patient is about to stop breathing. You must call for help and prepare to put in a breathing tube (intubation) immediately.
·Albuterol opens airways fast, but it does NOT stop the inflammation (swelling and irritation inside the airway walls). Systemic corticosteroids (prednisone by mouth or methylprednisolone by IV) cool down that inflammation and prevent symptoms from bouncing back 12 to 48 hours later. Give the steroid even if the patient feels better — it protects them over the next two days.
·Coughing is the body's way of clearing thick, sticky mucus plugs out of the airways. Blocking the cough traps that mucus inside and makes the airway blockage worse. Let the patient cough — it helps them breathe.
·During an asthma attack, airways are squeezed shut and filled with mucus — air gets TRAPPED inside the lungs and can't get out. Forcing deep breaths pushes more air in but doesn't let the old air escape, so the lungs overinflate like a balloon about to pop (this is called air trapping and dynamic hyperinflation). Let the patient breathe at their own pace. Give oxygen and bronchodilators to open the airways — that's what fixes the problem.

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