Hypoxia in Emergencies: How to Act?

Hypoxia occurs when the tissues receive an inadequate amount of O 2 . This leads to disruption of cellular function and a shift toward anaerobic metabolism and subsequent lactic acidosis may occur. While low O 2 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 concentration of O 2 in the blood, and depends largely on 5 key factors:

• Altitude : As the person moves to higher altitudes, the barometric pressure falls, leading to a decrease in the amount of inspired O 2 , despite a stable FiO 2 . At extreme altitude, the healthy lung would not have enough O 2 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 CO 2 . Hypoventilation leads to CO 2 accumulation, decreased CO 2 clearance, and subsequent decrease in alveolar O 2 concentration . In many disease processes, an increase in CO 2 itself can lead to increased work of breathing and is correlated 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 O 2 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 O 2 , since even poorly ventilated lung areas will receive adequate O 2 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 O 2 from reaching the alveoli and finally reaching the blood. In any case, a fraction of inspired O 2  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 O 2 carrying capacity .

Acute changes in hemoglobin level (such as acute blood loss anemia and hypovolemic shock) can lead to decreased O 2 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 O 2 (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 O 2 utilization by tissues. This can occur with direct cellular poisons (cyanide overdose, colchicine) or abnormally high tissue 0 2 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 SpO 2 , a major cause of hypoxia, and can be suspected in any patient with an O 2 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 O 2 saturation (SaO 2 ).

SaO 2 describes the amount of O 2 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 SaO 2 (SpO 2 ). 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), SpO 2 measurements should be taken with caution.

SpO 2 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 SpO 2 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 SaO 2 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 SaO 2 estimates , close to the 85%.

Care should also be taken when using pulse oximetry to measure SO 2 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. pulse and true SaO 2 .

New, multiwavelength pulse oximeters designed to measure methemoglobin and carboxyhemoglobin may improve future O 2 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 PaO 2 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 PaCO 2 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 (HCO 3 ).

Elevations in PaCO 2 with respect 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 PaCO 2 , base changes and HCO 3 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 PaO 2 , such as those with elevated levels of supplemental O 2 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, while GSV may be useful in detecting arterial hypercarbia, it correlates poorly with ABG results in pO 2 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.

>  Hypoxemic hypoxia:

• High altitude : high altitude pulmonary edema.
   
• Hypoventilation : central nervous system depressants (opioids), hypothyroidism, neuromuscular (myasthenia gravis, Guillain-Barré syndrome), nervous disease (cervical spine injuries, phrenic nerve injuries), chest wall injury (flail chest).
   
• Low Diffusion : pulmonary edema, pulmonary contusion, chronic obstructive pulmonary disease, interstitial lung disease.
   
• Ventilation/perfusion (V/Q) mismatch : pulmonary embolism, chronic obstructive pulmonary disease, asthma, mucosal plugging, pulmonary hypertension.
   
• Shunt : Intracardiac, arteriovenous malformation, pneumonia, atelectasis, acute respiratory distress syndrome.

>  Anemic hypoxia

• Acute blood loss anemia, hemorrhagic shock, carbon monoxide poisoning, methemoglobinemia.

>  Ischemic hypoxia

• Global : cardiogenic shock (myocardial infarction, heart failure), distributive shock (anaphylaxis, severe sepsis), obstructive shock (tamponade, tension pneumothorax), increased demand (seizures, chills).
   
• Local : arterial obstruction, interstitial edema.

>  Histotoxic hypoxia

• Cyanide poisoning, hydrogen sulfide

>  Maintain a patent airway

The first step in airway management is to evaluate whether the airway is patent . Hypoxic patients with respiratory failure or impaired consciousness may not be able to protect the patency of their airways, so endotracheal intubation may be warranted . Patients with respiratory failure who show signs of fatigue (such as lethargy, increased use of accessory muscles, decreased rate and depth of breathing) may decompensate without ventilatory support in whom intubation may also be warranted. Airway management is particularly important in inhalation injuries and comprehensive assessment and risk stratification of impending airway compromise can be performed with fiberoptic bronchoscopy.

>  Increase the oxygen content of inspired air

Supplemental oxygen is the cornerstone of therapy for many cases of hypoxia and can be divided into devices that provide low flow oxygen, high flow oxygen, and positive pressure ventilation . Supplemental oxygen at 100% FiO2 should be administered to any patient with suspected inhalation injury in whom the physiologic goal is to rapidly reverse and displace carbon monoxide from hemoglobin binding sites.

>  Positive Pressure Ventilation

Non-invasive positive pressure ventilation has well-studied indications for COPD exacerbations, acute asthma exacerbations, acute cardiogenic pulmonary edema, weaning from mechanical ventilation, respiratory failure and prevention of its worsening, and in patients with an order not to intubate. In these cases, positive ventilatory pressure functions physiologically to increase cardiac output, improve oxygen delivery, improve respiratory mechanics, and reduce respiratory effort. Endotracheal intubation should be considered in cases where non-invasive ventilation is contraindicated , such as in patients with altered mental status, vomiting, copious secretions, inability to protect the airway, upper airway obstruction.

>  Improve dissemination capacity

In acute cases of hypoxia due to underlying lung pathology, the general goal is to treat the underlying cause, which in some cases may involve improving oxygen diffusion across the alveolar-capillary membranes . Diuretics and pulmonary vasodilators may be considered in cases of pulmonary edema, and steroids may be considered in cases of interstitial lung disease. Extracorporeal membrane oxygenation ( ECMO) is the most invasive means of increasing oxygen diffusing capacity and its use is indicated in a subset of refractory cases of hypoxia.

Ultimately, acute cases of hypoxia require treatment of the underlying cause .

• Altitude sickness may require treatment with steroids and hyperbaric oxygen.
   
• Patients with severe hypoxia due to Acute Respiratory Distress Syndrome (ARDS) can be placed in the prone position to improve V/Q mismatch, improve oxygenation, and decrease mortality.
   
• The mainstay of therapy for cases of severe septic shock may include fluids, antibiotics, and medications to increase blood pressure.
   
• Patients with acute gastrointestinal blood loss and hemodynamic changes may require blood transfusions, particularly when hemoglobin levels reach 7 to 8 g/dL.
   
• In addition to oxygenation and ventilation support, patients with hypoxia from cardiogenic shock may require aggressive fluid management, vasopressor support, or placement of a mechanical circulatory support device.
   
• Hypoxia due to arterial ischemia and obstruction may require surgical consultation for percutaneous intravascular therapy.
   
• Hydroxocobalamin, a precursor of vitamin b-12, should be considered a first-line agent in the patient with suspected cyanide toxicity in whom the treatment binds to the toxic cyanide and forms a stable compound excreted in the urine.

•   Hypoxia is the inadequate supply of oxygen to tissues, and hypoxemia is just one of many causes.

•   In any patient with hypoxia who appears generally unstable , it is important to evaluate the patient’s AUC and vital signs.

•   There are many drawbacks to using pulse oximetry , and blood gas analysisis a more definitive tool in evaluating and managing a patient’s hypoxia.

•   While there are a variety of therapies to support and improve a patient’s oxygenation and ventilation, it is important to thoroughly investigate and treat the underlying cause in any patient with acute hypoxia.

•   Consider a broad differential diagnosis in cases of hypoxia that remain refractory to standard treatment.