• • Short + shallow: Neuromuscular, bronchospasm, or compliance problem → act fast ⚠️

  • Normal/large tidal volume: Compensation for metabolic/systemic cause

  • Use all tools: 👁 Eyes: Chest rise, ✋ Hands: Palpate,👂 Ears: Listen, 🧠 Brain: Synthesize

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In this episode, we focus on the bedside evaluation of the tachypneic patient. Tachypnea (increased respiratory rate) can be an early indicator of serious illness, but not every tachypneic patient is on the verge of arrest. The key is honing your bedside assessment to recognize who is at risk for rapid deterioration and why. We break down a practical approach you can use immediately at the bedside.

• Chest Rise:
  • Short, shallow respirations with poor chest rise are a major red flag.
  • Patients with minimal tidal volumes are often approaching respiratory failure.
• Diaphoresis and Tachycardia:
  • Diaphoresis + tachycardic patients with shallow breathing demand urgent attention as this is a sign of high catecholamine surge and impending respiratory collapse.
• Immediate Action:
  • Use your eyes (chest rise), your ears (stethoscope), and brain (putting together all of the pieces together)

1. Neuromuscular Disease
   • Myasthenia gravis crisis, Guillain-Barré, myopathies, frailty.
   • Weak inspiratory effort leads to low tidal volumes.
   • Needs urgent positive pressure support (BiPAP, or intubation).
2. Severe Bronchospasm
   • Asthma, COPD, anaphylaxis.
   • Shallow, forced expirations signal airway obstruction.
   • Silent Chest = airway emergency.
     • Treat with bronchodilators, steroids, and positive pressure ventilation.
     • Avoid immediate intubation if reversible; trial NIPPV first.
3. Worsening Lung Compliance
   • • • “Stiff lungs” harder to ventilate.
       • Compliance (C) = Δ Volume / Δ Pressure
       • So if it takes a lot of pressure to get adequate tidal volumes then your lungs are stiff and compliance is low
       • Causes include:
         • Chest Wall: Rigidity, burn eschar.
         • Pleural Space: Effusion, pneumothorax (check for asymmetric chest rise).
         • Lung Parenchyma: Pneumonia, contusion, atelectasis.
         • Below the Lung: Abdominal distension, ascites.
       • Clinical pearl: Work outside-in (chest wall, pleura, lung, abdomen).

1. Metabolic Acidosis (e.g., DKA)
   • Compensatory hyperventilation (Kussmaul breathing)
   • Check a blood gas (VBG/ABG) to differentiate gap vs. non-gap acidosis
2. Respiratory Alkalosis
   • Causes: Pain, anxiety, fever, early sepsis, CNS issues
   • Central drive increases respiratory rate
   • Again, ABG or VBG helps confirm
3. Dead Space Ventilation
   • Pulmonary embolism (PE) is the classic cause.
   • Other causes include:
     • Severe emphysema: Alveolar walls are destroyed, so air reaches areas with no capillary blood flow.
     • Pulmonary hypertension: High pressure damages and narrows vessels, reducing blood flow to ventilated alveoli.
     • Low-flow states (shock): Poor systemic perfusion limits blood reaching alveoli, creating ventilated but under perfused areas.
     • Excessive PEEP on ventilation: Overdistended alveoli compress nearby capillaries, blocking blood flow despite good ventilation
   • Key concept: Easy to oxygenate, but tachypneic due to perfusion/ventilation mismatch.

• Short, shallow breathing? Neuromuscular, bronchospasm, or compliance issue
  • Think: Impending respiratory failure, act quickly.
• Normal to large tidal volumes? Systemic causes
  • Think: Compensation (acidosis, pain, anxiety, PE).
• Use: Eyes (observe), Hands (palpate abdomen/chest), Ears (auscultate), Brain (synthesize).

A careful, simple bedside assessment can rapidly identify which tachypneic patients need immediate intervention—and help you avoid missing those headed toward respiratory collapse. Stay sharp, stay systematic!

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

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