Physiology

Respiratory Acidosis: Breathe Darn You!

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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

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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

Monro-Kellie and Their Doctrine: Blood, Brain, Spinal Fluid

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The Monro-Kellie doctrine states that three things exist within the fixed dimensions of the skull: blood, cerebrospinal fluid, and brain. An increase in any one component must necessarily lead to a decrease in one (or both) of the other components, otherwise intracranial pressure will increase.

Increases in one of the three components can take many different shapes and sizes. For example, abnormal bleeding within the cranium such as in epidural and subdural hematomas are common examples, which typically occur after traumatic events. Bleeding within the brain tissue itself – known as an intraparenchymal or intracerebral hematoma – can also occur, especially in patients with untreated high blood pressure. Brain tumors of any type effectively increase the amount of brain tissue. And last, but not least, the cerebrospinal fluid can back up in a condition known as hydrocephalus.

Regardless of the cause, the end result is an abnormal increase in either blood, brain, or cerebrospinal fluid within the confines of the skull.

So what’s the big deal? If the abnormality becomes large enough, the pressure within the skull can increase rapidly. Eventually the pressure can become so great that the brain gets squished, and will pop over rigid boundaries and out the small holes within the skull.

This is known as “herniating” the brain tissue. It can occur in numerous places depending on where the pressure is greatest. However, the most important herniation clinically occurs at the base of the skull where a hole known as the foramen magnum exists.

When the brain herniates here it really pisses off a vital structure known as the brainstem. The brainstem is responsible for all the stuff we don’t consciously think about (heart rate, breathing, etc.), which ultimately keeps us alive. When herniation of the brainstem through the foramen magnum occurs it stretches all the “wires” that allow our brainstem to function properly. If severe enough, all those autopilot functions (ie: breathing, beating of the heart, etc.) stop working and brain death occurs.

Overview

The skull contains three components within it: blood, brain, and cerebrospinal fluid. An abnormal increase in any one of these components causes an increase in pressure, which if severe enough, can cause herniation of brain tissue out of the skull. This can lead to coma and brain death.

References and Resources

Starling the Darling: Starling’s Equation and Fluid Movement

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Starling’s equation quantifies the movement of fluid into and out of a capillary as a result of filtration. It is based on two important variables: hydrostatic and oncotic pressure.

But before getting too scientific, let’s get back to the basics… Capillaries are the tinniest blood vessels in the body. They are the main site of gas and nutrient exchange for the tissues that they serve.

The fluid (ie: blood) inside the capillaries has a particular pressure associated with it. This is known as the “hydrostatic” pressure. In addition, there are numerous proteins floating around in the blood. These proteins determine the “oncotic” pressure.

Fluid, and to some degree proteins, are able to seep into and out of the capillary. However, the amount of “seepage” is based not only on the capillaries’ hydrostatic and oncotic pressure, but also on the hydrostatic and oncotic pressure of the surrounding tissues.

The tissue surrounding capillaries is composed of cells and their supporting structures. Depending on the particular tissue type, the supporting structures are generally proteins like collagen and long chain carbohydrate molecules known as proteoglycans. All of these molecules are collectively referred to as the “cellular interstitium”. The interstitium is where fluid seeps into and out of the capillary network.

The Equation

Taking the hydrostatic and oncotic pressures of the blood and interstitium into account we can predict which way fluid will move: in to or out of the capillary. This can be done numerically as shown in the following equation:

Driving pressure across capillary wall ≡
(PHS capillary – PHS interstitum) – (PO capillary – PO interstitium)

HS = hydrostatic pressure
O = oncotic pressure

If this number is positive, it means that fluid wants to leave the capillary and enter the interstitium (ie: there is a large driving pressure trying to push fluid out of the capillary); if it is negative, it means that fluid wants to leave the interstitium and re-enter the capillary.

Now to throw a monkey wrench into the equation… Although the hydrostatic and oncotic pressures are the main driving forces there are two additional factors that must be taken into account.

The first of these factors is the filtration co-efficient. It is based on how large and “leaky” the capillary wall is. Simply stated, if the capillary wall is large and leaky then more fluid can be filtered across it, duh! Increased leakiness can be caused by many different things such as histamine release (ie: allergies), mechanical damage to the capillary, etc.

The second factor that can alter the above equation is known as the reflection co-efficient. It is based on the fact that some proteins from the blood are able to cross the vessel wall into the interstitium. This effectively reduces the oncotic pressure within the capillary, and increases the oncotic pressure within the interstitium. Suffice it to say that different capillary beds have different reflection co-efficients depending on which organ system is being studied.

Taking everything into account we get the following equation:

Driving pressure across capillary wall ≡
Kf(PHS capillary – PHS interstitum) – σ(PO capillary – PO interstitium)

HS = hydrostatic pressure
O = oncotic pressure
Kf = filtration co-efficient
σ = reflection co-efficient

Overview

Starling’s equation predicts how much fluid will be filtered into, or out of, a capillary. It is based on four things: oncotic pressure, hydrostatic pressure, the reflection co-efficient, and the filtration co-efficient.

Related Articles

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Systemic Vascular Resistance: Radius, Length, Viscosity

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The systemic vascular resistance is the resistance that blood “sees” as it travels throughout the circulatory system of the body.

It is controlled by three different factors: length of the blood vessel (l), radius of the blood vessel (r), and the viscosity of the blood (η). The equation that relates these three factors to resistance is known as Poiseuilles’ equation:

R ≈ (η x l) / r4

Let’s discuss how each of the factors above influences resistance. The longer the vessel, the more likely blood will sludge and stick up against the walls; this tendency intuitively causes an increase in overall resistance. Blood vessel length does not typically change during adulthood, therefore its contribution to vascular resistance in humans is relatively constant.

When blood is more viscous than usual the resistance also increases. For example, molasses flows very slowly because it is highly viscous; blood is no different. There are a few uncommon instances in human physiology where blood viscosity increases; therefore, like vessel length, its contribution to vascular resistance is also relatively constant.

The most important parameter is the radius of the vessel. When the radius of a vessel shrinks, the resistance increases; when the radius of a vessel dilates, the resistance drops. Imagine trying to pump a set amount of fluid through a small opening versus a larger opening. There is much less resistance encountered through the larger opening. The same is true for large and small blood vessels. Even more importantly, as indicated by Poiseuille’s equation above, when the radius of a vessel is halved, the resistance increases by 16 fold! Therefore, even small changes in blood vessel diameter can have dramatic consequences on the bodies’ vascular resistance.

How the Body Controls Resistance

How do you think the body controls resistance most effectively? You guessed it! By controlling the radius of blood vessels. When there is an abnormal drop in vascular resistance, the body compensates by pumping out hormones (ie: epinephrine and norepinephrine); these hormones cause muscle cells surrounding blood vessels to constrict. Constriction leads to a decreased radius of the vessel, which leads to increased resistance.

Clinical Measurements

How do you measure systemic vascular resistance? Well, first off, systemic vascular resistance is not measured, but is calculated from other cardiovascular vital signs such as the mean arterial pressure (MAP), cardiac output (CO), and central venous pressures (CVP). The equation that relates these three values to resistance is:

SVR = [(MAP – CVP) / CO] x 80

Mean arterial pressure is a sort-of average between the systolic and diastolic blood pressure readings. It can be calculated using blood pressures obtained from an arterial catheter or a blood pressure cuff.

Central venous pressures are normally low, and do not contribute much to vascular resistance, but when very accurate measurements are needed they can be obtained from a central venous and/or a pulmonary artery catheter.

Cardiac output can be obtained from a pulmonary artery catheter if accurate values are needed; it can also be roughly estimated from a cardiac echocardiogram (ie: an ultrasound of the heart).

Role in Disease

So what’s the big deal? Why all this talk about vascular resistance? Vascular resistance is important because it is one determinant of blood pressure, and therefore organ perfusion.

The mean arterial pressure is calculated by multiplying the cardiac output by the systemic vascular resistance, and then adding the result to the central venous pressure (MAP = CO x SVR + CVP, a reorganization of the equation above).

Since the mean arterial pressure is the driving force behind the delivery of blood and oxygen to the organs, it is of vital importance that it stays above a certain threshold. Otherwise organs will not receive enough oxygen and will eventually die. One way of ensuring that the mean arterial pressure stays within a set range is for the body to constrict and/or dilate the vessels as needed.

On the flip side, if systemic vascular resistance is too "clamped" down then hypertension occurs. If severe enough, the heart may not be able to generate enough force to eject an adequate amount of blood into the tightened arterial system, which over time could result in systolic heart failure.

Overview

Systemic vascular resistance is the resistance blood sees as it travels throughout the bodies blood vessels. It is influenced by the length and radius of the blood vessel(s), as well as the viscosity of blood. It is calculated from the mean arterial pressure, central venous pressure, and cardiac output. Systemic vascular resistance plays a vital role in maintaining blood pressures within set ranges so that organ perfusion is maximized.

References and Resources