Pulmonary

Respiratory Acidosis: Breathe Darn You!

virtualmedstudent

A respiratory acidosis occurs when a person hypoventilates (ie: breathes too slow or too shallow). The result is an increase in PaCO2 (ie: the amount of CO2 dissolved in blood). The increase in plasma CO2 causes the blood to become acidic, which is manifest by a drop in the bodies’ pH. The reason blood becomes more acidic under these conditions is based on Le Chatelier’s principle. To understand this principle better let’s look at the equation that governs CO2 and HCO3– formation:

HCO3– + H+ <—> H2CO3 <—> CO2(g) + H2O

You’ll notice that CO2 (on the right most part of the equation) is what is exhaled via the lungs. When a patient is hypoventilating there is more CO2 than normal in the blood stream. The body compensates by turning this CO2 into HCO3– and H+. The resulting increase in H+ causes the acidosis (decrease in pH).

Causes

What causes someone to hypoventilate? There are many causes! All of them relate to a decreased ability of the patient to breath at a rate sufficient to remove carbon dioxide from the blood stream.

Medications that slow respiratory rate (ie: morphine and other pain medications) are notorious culprits. Poor pulmonary mechanics from obesity or neuromuscular disease (ie: amyotrophic lateral sclerosis) can also cause decreased respiratory rates. Lung and chest wall diseases are also common causes of respiratory acidosis and include pneumonia, pneumothorax, and decreased respiratory rate secondary to pain from rib fractures.

When assessing someone who has a respiratory acidosis ask this question first: what is causing the patient to have a decreased respiratory rate? Look for signs of external chest wall trauma, pneumonia, etc. Look through the medication record (how much pain medication have they gotten?) to get an idea of what medications could be causing their decreased ventilatory drive.

In general, the most common causes of hypoventilation are:

  • Medicines (especially pain medications)
  • Airway obstruction
  • Central nervous system disease (ie: diaphragmatic paralysis from cervical spinal cord trauma)
  • Chest wall problems (pneumo/hemothorax, flail chest, broken ribs, etc.)
  • Nerve and muscle diseases
  • Lung diseases (ie: pneumonia, restrictive lung diseases, etc.)

Acute Versus Chronic and Kidney Compensation

A respiratory acidosis can be either acute or chronic. The difference depends on how much the kidney compensates for the change in pH. How exactly does the kidney compensate? It decreases its secretion of HCO3– (aka: bicarbonate ion) into the urine. This helps offset the acidosis, and brings the bodies pH back towards normal limits.

How do we determine if the kidney is acutely or chronically compensating? We measure the bicarbonate level (one of the results in a "chemistry panel"). The kidney is acutely compensating if the HCO3– level is increased 1 to 2 mmol/L per every 10 mmHg increase in the PaCO2 level (normal PaCO2 level is 40 mmHg). The kidney is chronically compensating if the HCO3– level is increased 3 to 4 mmol/L per every 10 mmHg increase in PaCO2.

For example, if a patient’s PaCO2 on blood gas analysis is found to be 60 mmHg (a normal level is 40) we would say there is a 20 mmHg increase present (ie: the patient is unable to eliminate 20 mmHg of excess CO2 from the blood stream via the lungs). If the HCO3– (determined by a chemistry panel) is at 27 (for argument sake we’ll say a normal bicarbonate level is 23) then that represents a 4 mmol increase in the bicarbonate level for the 20 mmHg increase in CO2, or approximately 2 mmol increase in bicarb per 10 mmHg increase in CO2. This would mean the patient’s kidney is acutely compensating for the respiratory acidosis.

  Bicarbonate Level (HCO3–)
Acute Kidney Compensation Increased by 1-2 mmol/L for every 10 mmHg increase in the PaCO2
Chronic Kidney Compensation Increased by 3-4 mmol/L for every 10 mmHg increase in the PaCO2

Why is it important to determine if acute or chronic kidney compensation is occurring? For starters, it gives the clinician a better idea of what may be causing the respiratory acidosis.

If the kidney is acutely compensating we know that the problem is new. The patient is likely having an acute issue (ie: trauma to the chest that caused multiple rib fractures). If the compensation is chronic then we know that the patient has been breathing at a slower than normal rate for a prolonged period of time. This may be seen in long standing neuromuscular diseases that cause poor pulmonary mechanics, obesity, etc.

Treatment

Treatment is straightforward: eliminate the underlying cause! If the patient received too much morphine give some naloxone to wake them up. Sometimes patients cannot maintain an adequate respiratory rate on their own, and mechanical ventilation is required. Once the patient is adequately ventilated the respiratory acidosis should resolve.

Overview

A respiratory acidosis occurs when a patient is unable to remove CO2 from the bloodstream secondary to a decreased respiratory rate (ie: hypoventilation). There are numerous causes including neuromuscular diseases, pain medication, and chest trauma. The kidney can acutely or chronically compensate for a respiratory acidosis depending on how long it has been present. Treatment is to fix the underlying cause.

You Are Just Getting Started… Learn Some More!

References and Resources

Respiratory Alkalosis: PaCO2 and Some Rapid Breathing

virtualmedstudent

A respiratory alkalosis occurs when a person breathes too rapidly. The result is a decrease in PaCO2 (ie: the amount of CO2 dissolved in the blood). This causes the blood to become alkalotic (less acidic), which is manifest by an increase in the blood’s pH. The reason the blood becomes less acidic is based on Le Chatelier’s principle. If we take a look at the following equation:

HCO3– + H+ —> H2CO3 –> CO2(g) + H2O

You’ll notice that CO2 (on the right most part of the equation) is what is exhaled via the lungs. When a patient is hyperventilating there is much less CO2 than normal in the blood stream. The body compensates by combining HCO3– and H+ to form more CO2. The resulting decrease in H+ causes the alkalosis (ie: rise in pH).

Causes of Respiratory Alkalosis

So what could cause someone to hyperventilate? The most common things are pain, anxiety, and fever. If the patient is in the ICU and being mechanically ventilated then a respiratory alkalosis may develop if the ventilator is set to give too many breaths per minute.

The most common causes of hyperventilation are:

  • Fever
  • Pain
  • Anxiety
  • Overventilating a mechanically ventilated patient

Acute Versus Chronic and Kidney Compensation

A respiratory alkalosis can be either acute or chronic. The difference depends on how much the kidney compensates for the change in pH. How exactly does the kidney compensate? It dumps HCO3 (aka: bicarb) into the urine. This helps offset the alkalosis and brings the bodies pH back to normal limits.

How do we determine if the kidney is acutely or chronically compensating? We measure the bicarb level. The kidney is acutely compensating if the HCO3 level is decreased 1 to 2 mmol/L per every 10 mmHg drop in the PaCO2 level. The kidney is chronically compensating if the HCO3 level is decreased 4 to 5 mmol/L per every 10 mmHg drop in PaCO2.

For example, if a patient’s PaCO2 on blood gas analysis is found to be 20 mmHg (a normal level is around 40) we would say there is a 20 mmHg drop present. If the HCO3 (determined by a chemistry panel) is at 19 (for argument sake we’ll say a normal bicarbonate level is 23) then that is a 4 mmol drop in the bicarb level for the 20 mmHg drop in CO2, or approximately 2 mmol drop in bicarb per 10 mmHg drop in CO2. This would mean the patient’s kidney is acutely compensating for the respiratory alkalosis.

  Bicarbonate Level (HCO3)
Acute Compensation Decreased by 1-2 mmol/L for every 10 mmHg decrease in the PaCO2
Chronic Compensation Decreased by 4-5 mmol/L for every 10 mmHg decrease in the PaCO2

Why is it important to determine if acute or chronic compensation is occurring? For starters, it gives us a better idea of what may be causing the respiratory alkalosis. If the kidney is acutely compensating we know that the respiratory alkalosis is new. The patient is likely having an acute reaction to something (ie: pain, anxiety, panic attack, etc.). If the compensation is chronic then we know that the patient has been breathing at a faster than normal rate for a prolonged period of time. This may be seen in pregnancy, COPD, and emphysema.

Treatment

Treatment is very straightforward: eliminate the underlying cause! If the patient appears in pain then give pain medication. Fever? Hit them with some acetaminophen. If the patient is mechanically ventilated then decrease the respiratory rate. Once the stimulus for hyperventilating is removed the respiratory alkalosis should improve.

Overview

A respiratory alkalosis occurs when a patient is breathing too rapidly, which cause too much CO2 to be removed from the bloodstream. There are numerous causes including anxiety, pain, and fever. The kidney can acutely or chronically compensate for a respiratory alkalosis depending on how long it has been present. Treatment is to fix the underlying cause.

A Little More Learning…

References and Resources

Pneumothorax: Visceral and Parietal Pleura and a Little Air In Between

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In order to understand what a pneumothorax is we have to first appreciate the anatomy of the lung and its surrounding tissues.

The lung is enveloped by two layers of connective tissue known as the visceral and parietal pleura. The visceral pleura is directly connected, and immediately adjacent to the lungs. The parietal pleura sits on top of the visceral pleura like a blanket, but is not, in the strictest sense of the word, attached to the visceral pleura.

This unique arrangement creates a potential space between the visceral and parietal layers. Normally this space is empty and the layers of pleura sit directly on top of one another. However, in some instances air can dissect into that potential space. When this occurs it is called a “pneumothorax”.

Classification

A pneumothorax is classified as either “simple” or “tension”. A tension pneumothorax occurs when a progressively larger amount of air gets trapped in the space between the parietal and visceral pleural layers.

Tension pneumothoraces occur when the pathology causing the pneumothorax creates a one way valve mechanism allowing air into, but not out of the pleural space. With each breath more air is drawn into the pneumothorax, but is unable to escape. The end result is progressive enlargement of the pneumothorax. As a result, the air pushes the heart and mediastinal structures to the opposite side of the chest. And this is no bueno.

On the other hand, a simple pneumothorax is present when the amount of air remains stable, and there is no shift of mediastinal structures.

Causes

Anything that introduces air between the parietal and visceral pleura can cause a pneumothorax. Trauma is a common cause of pneumothorax and can occur if the chest wall is damaged or a bronchus ruptures. Subpleural blebs, which are basically small “air blisters” on the surface of the lung are also common causes of non-traumatic pneumothorax. Patients who smoke, or who have underlying connective tissue diseases such as Marfan’s syndrome are at increased risk of developing a pneumothorax. For unclear reasons, spontaneous pneumothorax is often seen in tall, thin, white males.

Signs and Symptoms

Signs and symptoms are usually dependent on the size of the pneumothorax. One common symptom is “pleuritic” chest pain. This is caused by air irritating the parietal pleura; this type of pain is usually worse when the patient takes a breath. Patients also commonly complain of dyspnea (ie: shortness of breath).

On physical exam the patient will have decreased or absent breath sounds over the area of the pneumothorax. In addition, if you percuss (ie: tap) the patient’s lung with your finger it will sound hyper-resonant. In tension pneumothoraces the air may push on heart structures leading to tachycardia (ie: increased heart rate) and hypotension (ie: decreased blood pressure).

Diagnosis

The quickest way to diagnose a pneumothorax is with a chest x-ray. There are several things you should look for when attempting to diagnose a pneumothorax based on an x-ray.

The first is absence of lung markings. However, this is not a fool proof system because lung markings may be absent in other diseases of the lung such as bullae. You also need to see a white line that parallels the chest wall. This is known as the "pleural white line", which represents separation of the visceral and parietal pleura. Additionally, in a tension pneumothorax the heart structures and trachea will deviate away from the pneumothorax.

Treatment

Treatment is dependent on the size of the pneumothorax and whether or not the patient has symptoms. Small (ie: less than 3cm between the chest wall and lung tissue) and asymptomatic lesions can be treated conservatively with supplemental oxygen via a nasal cannulae or face mask.

If the pneumothorax is larger than 3cm, or the patient has symptoms, a needle can be used to aspirate the air out of the chest. If this fails to re-inflate the lung, the patient will likely have to have a chest tube placed. In addition, any patient who is clinically unstable should have a chest tube placed.

Tension pneumothoraces are treated emergently by inserting a large bore needle into the 2nd intercostal space at the midclavicular line. This allows trapped air to escape through the newly created needle hole and prevents further air trapping.

Overview

A pneumothorax occurs when air dissects between the visceral and parietal pleural layers that envelope the lung. There are numerous causes. Symptoms include chest pain and shortness of breath although small pneumothoraces may be asymptomatic. Diagnosis is generally made from a chest x-ray. Treatment depends on symptomatology and the size of the pneumothorax.

References and Resources