Vomiting (Emesis) Physiology

Vomiting is a protective reflex that forcefully expels gastric (and sometimes duodenal) contents. It is coordinated centrally and executed through a precise sequence of visceral and somatic motor events.

1. Central Coordination — The Vomiting Center

A vomiting center in the medulla coordinates the entire reflex. It receives afferent (sensory) input from four main sources:

Vestibular system (explains motion sickness)
Oropharynx ("back of the throat" — mechanical/chemical irritation, gag stimulation)
Gastrointestinal tract (vagal and sympathetic afferents from mucosal irritation, distension, or toxins)
Chemoreceptor trigger zone (CTZ) in the floor of the fourth ventricle

The CTZ is important because it lies outside the blood-brain barrier, allowing it to directly sense circulating toxins, drugs, and metabolic byproducts (e.g., chemotherapy agents, opioids, uremia) and relay that signal to the vomiting center. Clinically, the CTZ is rich in dopamine (D2), serotonin (5-HT3), and neurokinin (NK1) receptors, which is why antiemetics like ondansetron (5-HT3 antagonist), metoclopramide/prochlorperazine (D2 antagonists), and aprepitant (NK1 antagonist) work.

(Source: Costanzo Physiology, 7th Edition, p. 359-360)

2. The Vomiting Reflex — Temporal Sequence of Events

Once triggered, the vomiting center orchestrates a fixed, stereotyped sequence:

Abolition of gastric and small intestinal slow-wave activity — normal peristalsis stops
Retrograde (reverse) peristalsis — begins in the small intestine and sweeps contents upward into the stomach
Relaxation of the stomach and pylorus — the stomach becomes a receptive reservoir rather than a propulsive organ
Forced inspiration against a closed glottis — sharply increases intra-abdominal pressure, which compresses the stomach
Upward and forward movement of the larynx, with relaxation of the lower esophageal sphincter — opens the pathway from stomach to esophagus
Closure of the glottis — protects the airway from aspiration
Forceful expulsion of gastric (and sometimes duodenal) contents through the mouth

(Source: Costanzo Physiology, 7th Edition, p. 360)

3. Retching vs. True Vomiting

An important distinction: in retching, the upper esophageal sphincter stays closed while the lower esophageal sphincter is open. This means gastric contents are propelled into the esophagus but, because the upper sphincter doesn't open, they fall back into the stomach once the retch ends — no expulsion occurs. True vomiting requires both sphincters to open in coordinated sequence for actual expulsion.

Clinical Relevance

This physiology explains several therapeutic principles:

Because multiple afferent pathways converge on the vomiting center, combination antiemetic therapy (e.g., a 5-HT3 antagonist + dexamethasone + NK1 antagonist for chemotherapy-induced nausea/vomiting) is often more effective than single-agent therapy, since different triggers act through different receptors.
Vestibular-mediated vomiting (motion sickness) responds best to antihistamines/anticholinergics rather than dopamine antagonists, since it bypasses the CTZ.
Because expulsion requires airway closure timed with LES relaxation, impaired consciousness (e.g., sedation, intoxication) creates high aspiration risk if the reflex sequence is incomplete or protective reflexes are blunted.

A recent evidence check for postoperative nausea/vomiting management (not physiology per se) found relevant meta-analyses: early oral intake post-anesthesia (PMID: 40178470), chewing gum for postprocedural nausea (PMID: 38206218), and gastric aspiration after oral/maxillofacial surgery (PMID: 38363948) — these address prevention strategies rather than contradicting the core physiology above.

pulse oximetery

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"pulse oximetry"[MeSH Terms] AND accuracy

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Pulse Oximetry

Basic Principle

Pulse oximetry is a noninvasive method for continuously estimating the oxygen saturation of arterial blood (SaO2, displayed as SpO2). It works by dual-wavelength spectrophotometry:

A probe (typically on a finger, earlobe, or nose) shines light at two wavelengths - commonly 660 nm (red) and 940 nm (infrared) - through the tissue to a sensor on the other side.
Oxyhemoglobin and deoxyhemoglobin have different light absorption spectra: deoxyhemoglobin absorbs more red light, while oxyhemoglobin absorbs more infrared light.
The device measures the ratio of absorbance at the two wavelengths and calculates the percent saturation of hemoglobin.

(Costanzo Physiology, 7th Ed., p. 226; Schwartz's Principles of Surgery, 11th Ed., p. 474)

Why It Measures Only Arterial Saturation

Skin, venous blood, and capillary blood also absorb light, but they don't pulse. Arterial blood pulses with each heartbeat, causing a small, rhythmic change in the light absorbance signal. The oximeter isolates this pulsatile component and subtracts out the constant "background" absorbance from tissue, venous, and capillary blood - which is how it selectively reports arterial saturation rather than a mixed venous-arterial value. This is why a pulse oximeter needs a detectable pulse (poor peripheral perfusion, hypotension, or vasoconstriction can give inaccurate or unreadable results).

(Costanzo Physiology, 7th Ed., p. 226)

Important Point: It Does NOT Measure PaO2 Directly

Pulse oximetry reports % saturation, not the partial pressure of oxygen (PaO2). You can estimate PaO2 from the SpO2 using the oxygen-hemoglobin dissociation curve, but the relationship is not linear - the curve is sigmoidal, so at saturations above ~90%, large changes in PaO2 produce only small changes in SpO2. This means pulse oximetry can miss significant drops in PaO2 while SpO2 still looks reassuring, especially on the flat upper part of the curve.

Clinical Utility

One of the most widely used continuous, noninvasive monitoring tools in anesthesia, critical care, and general ward settings.
Used routinely in intubated/mechanically ventilated patients, during sedation, and in patients with respiratory disease.
Helps titrate FiO2 and PEEP, and guides weaning from mechanical ventilation.
Has reduced the need for frequent arterial blood gas sampling, and continuous monitoring in surgical patients is associated with reduced unrecognized deterioration, rescue events, and ICU transfers.

(Schwartz's Principles of Surgery, 11th Ed., p. 474)

Key Limitations and Sources of Error

Carboxyhemoglobin (CO poisoning): The device cannot distinguish carboxyhemoglobin from oxyhemoglobin, so it falsely reads SpO2 as normal/high even when true oxygen-carrying capacity is severely reduced. Co-oximetry (multi-wavelength) is needed to detect this.
Methemoglobinemia: When methemoglobin is markedly elevated, the oximeter characteristically reads a fixed ~85% regardless of true saturation.
Accuracy declines at low saturations: Accuracy starts to degrade below SaO2 of ~92% and becomes unreliable below ~85%.
Poor perfusion states: Hypotension, peripheral vasoconstriction, cold extremities, or motion artifact can prevent an adequate pulsatile signal.
Nail polish, dyes (e.g., methylene blue), and ambient light can interfere with the signal.
Skin pigmentation: This is an active area of concern - recent systematic reviews and meta-analyses have found that pulse oximeters can overestimate true arterial oxygen saturation in patients with darker skin pigmentation, increasing the risk of missed hypoxemia in these patients. This is a clinically important and ongoing safety issue that is not covered in older textbook editions.

(Schwartz's Principles of Surgery, 11th Ed., p. 474)

Recent Evidence Worth Flagging

Two recent systematic reviews/meta-analyses reinforce the skin-pigmentation accuracy problem and should inform clinical interpretation of SpO2 in darker-skinned patients:

Martin et al. 2024, British Journal of Anaesthesia - systematic review on the effect of skin tone on pulse oximetry accuracy (PMID: 38368234)
Singh et al. 2024, JMIR - systematic review/meta-analysis on skin pigmentation's impact on pulse oximetry and wearable pulse rate accuracy (PMID: 39388258)

Both support using clinical judgment (and arterial blood gas confirmation when in doubt) rather than relying on SpO2 alone in patients with darker skin, particularly near borderline saturation thresholds.

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