Streamlining the Management of Hypoxia in Emergency Room Settings

Hypoxia occurs when the tissues receive an inadequate amount of O2. This leads to disruption of cellular function and a shift toward anaerobic metabolism and subsequent lactic acidosis may occur. While low O2 in the blood, also known as hypoxemia , is one of the main causes of hypoxia, it is not the only one.

Hypoxia can best be divided into 4 main categories:

• Hypoxemia
• Anemic hypoxia
• Ischemic/stagnant hypoxia
• Histotoxic hypoxia

It is hypoxia that refers to the state of low O2 concentration in the blood, and largely depends on 5 key factors:

• Altitude : As the person moves to higher altitudes, the barometric pressure drops, leading to a decrease in the amount of inspired O2, despite a stable FiO2. At extreme altitude, the healthy lung would not have enough O2 in the inspired air to be adequately supplied to tissue metabolism.
   
• Ventilation : Ventilation refers to the supply of gases to the alveoli and is directly related to the removal of CO2. Hypoventilation leads to CO2 accumulation, decreased CO2 clearance, and subsequent decrease in alveolar O2 concentration. In many disease processes, an increase in CO2 itself can lead to increased work of breathing and correlates with lung compliance and airway resistance. For example, a patient with an acute exacerbation of asthma will have elevated airway resistance, exacerbating the work of breathing.
   
• Oxygen diffusion : It is the ability of O2 to pass through the alveoli and surround the capillary membranes effectively. Transport may be affected by a primary tissue pathological process, such as in pulmonary fibrosis.
   
• Ventilation/perfusion (V/Q) matching: There is a balance between oxygenation of the alveoli and blood flow through their capillaries. The discrepancy between these two factors will appear when blood flows through inadequately ventilated alveoli or does not reach adequately ventilated alveoli. Examples of this are pulmonary embolism, in which perfusion is obstructed, and status asthmaticus, in which collapse of the airways causes air trapping and obstruction of ventilation. The imbalance can be corrected by inhaling excess O2, as even poorly ventilated lung areas will receive adequate O2 flow. It is important to note that, in the normal state, ventilation/perfusion matching is heterogeneous in different areas of the lung, and that it is exacerbated under certain conditions that affect V/Q mismatch (e.g., asthma, pneumonia). .
   
• Bypass or short circuit of blood : refers to the short circuit of the process by which the blood receives oxygenation. In other words, blood enters the systemic circulation before receiving adequate oxygenation. Classic examples of bloodstream shunting occur with anatomical defects such as those of the interventricular septum. Another example is the presence of a mucous plug in a main bronchus, which will prevent O2 from reaching the alveoli and finally reaching the blood. In any case, a fraction of inspired O2 will not fill the alveoli that are receiving blood, and therefore, hypoxemia will not be corrected.

Hypoxia can occur if the blood has a critically low O2 carrying capacity.

Acute changes in hemoglobin level (such as acute blood loss anemia and hypovolemic shock) can lead to decreased O2 transport to tissues. Hypoxia can also result from changes in hemoglobin functionality , such as in acute carbon monoxide poisoning , where there are many hemoglobin molecules that simply cannot bind oxygen.

Hypoxia may result from a critical decrease in the flow of oxygenated blood to peripheral tissues.

Systemic conditions, such as cardiogenic shock, can lead to decreased blood oxygenation during pulmonary gas exchange, as well as inadequate overall blood supply to central and peripheral organs. Localized conditions may impede cellular diffusion of O2 (as in severe tissue edema) or focally impede the flow of oxygenated blood (as in arterial damage or obstruction).

Hypoxia may be due to low O2 utilization by tissues. This can occur with direct cellular poisons (cyanide overdose, colchicine) or abnormally high tissue 02 demand (malignancy).

Although there is no single laboratory value to directly measure hypoxia, it should be suspected in any patient with anxiety, confusion, and restlessness, which may be early signs of hypoxia and may precede changes in vital signs.

The hallmark of hypoxemia is low SpO2 , a major cause of hypoxia, and can be suspected in any patient with an O2 saturation <90% (or <88% in patients with chronic lung disease).

Lactic acidosis may develop in response to anaerobic metabolism, tissue hypoxia, or increased catecholamine surge, and may be detected on blood gases.

1-  Patient stability : check general condition and vital signs. Critical to decision making for any patient in the ED is a quick but thorough assessment to determine whether the person is “sick or not sick.”

> General condition

What does the patient look like? Is he comfortable or in a state of acute distress? Does the patient display any behavior that could be a clinical sign, however subtle, of “abnormality”?

> Evaluation of airways, breathing and circulation

In any patient who may be experiencing critical illness (including hypoxia) it is appropriate to evaluate the airway, breathing, and circulation.

Is the patient protecting his or her airway? Although rare, hypoxia may be due to critical narrowing of the airways leading to stridor on lung auscultation. In children, the presence of laryngeal stridor requires a search for upper airway obstruction. Hypoxia may be seen from severe smoke inhalation injury, which may present with rales and snoring, and lead to imminent airway compromise.

Are breath sounds present bilaterally?

While tension pneumothorax is associated with classic symptoms of respiratory distress and tracheal deviation, only half of cases may present with frank hypoxia.

Does the chest wall rise and fall equally?

Patients with significant rib fractures resulting in an unstable chest wall may have inadequate ventilation and develop hypoxia, as well as hypercapnia and acidosis.

Is the patient tachycardic? Are distal pulses present?

Threadlike pulses may indicate intravascular volume loss. In the patient with blunt trauma, this may be a manifestation of hemorrhagic shock, and resuscitation is vital to prevent tissue hypoxia. In the patient with severe infection, tachycardia may be the manifestation of fluid changes mediated by inflammation and subsequent target organ hypoperfusion and ischemic damage.

> Vital signs

In any unstable patient it is crucial to obtain a complete set of vital signs, which are likely abnormal and may help elucidate the underlying etiology of the patient’s instability.

Acute hypoxia is more likely to manifest with an increased respiratory rate (>24) and an increased heart rate (>100), but normal respiratory rate and heart rate should not exclude the possibility of hypoxia. .

In diseases with hypoxemia and hypercapnia , in addition to the respiratory rate, the body will try to increase the tidal volume with the aim of increasing alveolar ventilation. Patients with abrupt loss of intravascular volume may develop tachycardia and hypotension and, as hypovolemia worsens, increase respiratory rate to compensate for subsequent tissue hypoxia.

Patients with arterial hypotension may have hypoxia due to poor perfusion and warrants prompt investigation of the underlying cause. Hypoxic patients from septic shock may be hyperthermic or hypothermic. This can be best identified by measuring core temperature (such as rectal temperature).

Pulse oximetry readings are prone to inaccuracies , especially in unstable patients, and should always be considered in a clinical context.

2- History and physical examination

In the unstable patient , the history may be limited. However, in the stable patient it is important to take a complete medical history and physical examination, this being the first important step.

Does the patient have a history of heart or lung disease ?

Patients with pre-existing cardiovascular disease are more likely to develop end-organ hypoperfusion and a subsequent hypoxic state.

Patients with underlying lung disease are prone to develop physiologic changes that increase the risk of hypoxemia and subsequent hypoxia, including decreased ventilatory drive, obstructive airway processes, intraalveolar exudates, alveolar septal thickening, inflammation and fibrosis, and damage to the lungs. alveolocapillary.

Is there a history of smoking?

Smoking is associated with a greater risk of hypoxia, due to the physiological alteration of lung function. Blood carbon monoxide levels are often elevated in chronic smokers, in whom severe elevations and symptoms of hypoxia have been reported.

Recent surgeries?

In the postoperative period , patients are more prone to suffer atelectasis, pneumonia and pulmonary embolism, pathologies that can cause hypoxia.

Review of systems : Many patients with hypoxia present with dyspnea or increased work of breathing, but also confusion or a feeling of sluggishness. Headache may be the only symptom of hypoxia in patients with acute carbon monoxide (CO) poisoning.

> Physical examination

The general appearance of the patient can guide the etiology.

• Cyanosis may first appear on the lips and distal fingertips and be a sign of severe hypoxemia . Diffuse, dull, red skin discoloration may be a sign of cyanide toxicity.
   
• Paleness may be a sign of anemia due to acute blood loss.
   
• Crackles on lung auscultation may indicate heart failure if bilateral or lobar pneumonia if focal and unilateral.
   
• The absence of breath sounds may indicate a stroke or collapsed lung.
   
• The distal extremities may be warm in distributive shock or cold and clammy in a patient with hemorrhage.
   
• Cherry red skin and mucous membranes are common postmortem findings in poisoning ; in fact, they are rare at presentation.
   
• The patient may be upset and restless on neurological examination .

The gross appearance of blood on rectal examination may indicate anemia due to acute blood loss.

3-  Additional evaluation

> Arterial O2 saturation (SaO2).

SaO2 describes the amount of O2 bound to hemoglobin, and normal values ​​range between 95% and 100%.

A quick way to evaluate this is with pulse oximetry . Based on the known absorption of light at particular wavelengths of oxygenated and deoxygenated blood, pulse oximetry uses spectrophotometry to calculate estimated SaO2 (SpO2). The accuracy of this measurement depends in part on the precise strength of the signal translated into a waveform, which should normally be sharp, with a clear dicrotic notch.

Low perfusion states will have low amplitude sinus waveforms. In these patients (such as those with low cardiac output, peripheral vasoconstriction, or hypothermia), SpO2 measurements should be taken with caution.

SpO2 readings should also be taken with caution in patients with nail polish, which can significantly interfere with light absorption at the wavelengths used by pulse oximetry, as well as in patients with darker skin pigmentation.

It is important to note that SpO2 is often inaccurate in patients with CO poisoning. In fact, since oxyhemoglobin and carboxyhemoglobin have similar absorption properties for red light, in patients with CO poisoning; pulse oximetry will often estimate true SaO2 as normal or falsely elevated; This absorption property is also the reason why patients with CO poisoning appear cherry red.

Methemoglobinemia is another disease in which its red light absorption properties will make pulse oximetry unreliable and is the reason why significant toxicity often changes pulse oximetry SaO2 estimates by around 85 %.

Caution should also be used when using pulse oximetry to measure SO2 trend in critically ill patients, in whom the effects of acidosis and anemia have been shown to interfere with the correlation of pulse oximetry estimates. and true SaO2.

New, multiwavelength pulse oximeters designed to measure methemoglobin and carboxyhemoglobin may improve future O2 monitoring capabilities.

> Arterial blood gas analysis (ABG)

The ABG analysis provides information on alveolar ventilation, oxygenation, and acid-base balance.

In assessing these key physiological processes, ABGs measure the partial pressure of arterial O2 (PaO2) and CO2 (PaCO2) and, compared to pulse oximetry, is a more definitive tool for assessing oxygenation and ventilation. Normal PaO2 is between 80 and 100 mmHg and, as a cause of hypoxemia, lower values ​​may indicate hypoxia . Knowledge of its value is also useful in the management of patients on ventilatory support.

Normal PaCO2 is considered 35 to 45 mmHg, and its levels may be elevated in situations of increased metabolism or decreased ventilation ; In any case, the acuity of hypercapnia can be assessed on the basis of any concurrent changes in the bicarbonate ion (HCO3).

Elevations in PaCO2 relative to baseline in respiratory distress associated with increased work of breathing may indicate respiratory failure and serve as an indication for ventilatory support. While most ABG assays directly measure pH and PaCO2, base changes and HCO3 are calculated indirectly; especially in critically ill patients. These latter calculations can be highly variable and should be interpreted with caution.

This rapid and direct measurement of pH can be essential in patients with metabolic disorders, such as severe sepsis, diabetic and alcoholic ketoacidosis, trauma, acute respiratory failure, cardiac arrest, and COPD. In these situations, venous blood gas (VBG) analysis, which may be clinically preferred for numerous reasons, is also reliable.

It is imperative to always interpret GSAs within the patient’s clinical context.

The accuracy of data collected from an ABG sample is particularly susceptible to error, and care must be taken to confirm that the blood sample is truly arterial (and not venous) in nature, completely and quickly remove any air bubbles. , inspect for clots, and have the sample analyzed within 30 minutes of the collection time.

ABG sampling is even more prone to error in patients with elevated PaO2, such as those with elevated levels of supplemental O2 or in whom arterial shunt physiology is suspected, as well as patients with leukocytosis or thrombocytosis. The ABG test should be performed within 5 minutes.

> Venous blood gas analysis (GSVV )

Compared with ABGs, puncture for GSV is typically quicker to perform, less painful, and carries a lower risk of complications such as arterial injury and thrombosis. Because of these potential benefits, when establishing acid-base status and evaluating respiratory function in the ED, GSV analysis should be considered. This assay is noninferior in its ability to detect acid-base abnormalities in critical diseases such as coronary artery disease and acute exacerbations of COPD.

Caution should be used in severe hemodynamic compromise, such as in severe shock or cardiac arrest, when venous blood lactate and pH analysis has been shown to be less reliable.

Furthermore, although GSV may be useful in detecting arterial hypercarbia, it correlates poorly with ABG results in pO2 and pCO2 analysis, and is too clinically unpredictable.

> Images

Chest imaging can help determine the underlying cause of hypoxia.

Chest x-ray may be useful in diagnosing focal airway disorders, such as pneumonia, acute respiratory distress syndrome, pulmonary hyperinflation, and pulmonary edema. An initial chest x-ray cannot always elucidate an underlying etiology.

Chest CT may be helpful to provide more details. Evidence of smoke inhalation injury may be absent on the initial chest x-ray, but will serve as an initial evaluation in such cases.

> Case 1

This patient had platypnea-orthodeoxia syndrome (POS), a disease characterized by positional dyspnea (platypnea) and hypoxemia in the upright position (orthodeoxia). Unlike orthopnea, it is relieved by lying down. The underlying cause of it was shunting of blood through a patent foramen ovale, which is the most common cause of POS. In general, POS occurs in elderly patients with anatomical cardiac defects who later in life have developed new secondary anatomical or functional abnormalities, leading to clinically significant blood shunt physiology and subsequent hypoxemia. This case highlights the need to maintain a high level of suspicion in cases refractory to standard treatment.

> Case 2 :

This patient had congenital methemoglobinemia, which was not evident at birth due to the phenomenon of hemoglobin change. Otherwise, healthy people have a small amount of methemoglobin. This disease is characterized by a deficiency in cytochrome b5 reductase (b5R), which alters the biochemical pathway responsible for reducing methemoglobin to normal hemoglobin in the blood. It was noted that the patient had a parent with a similar disease. Methemoglobinemia should be suspected in any patient with cyanosis and abnormal SpO2 who does not respond to supplemental O2. It is not always detected by pulse oximetry and requires an ABG analysis, which demonstrated a methemoglobin concentration of 10.6%. Formal diagnosis is made with DNA sequencing. The primary treatment for methemoglobinemia is methylene blue and should be administered 1-2 mg/kg IV.