[Clinical Art][Circulation] Interpretation of Hemodynamic Waveforms

October 20, 2016 Cardiology, Critical Care, EKG/ECG, Hemodynamics, Mechanical Ventilation No comments , , , , , , , , , , , , , , , , , , , , , , , , ,

1st_ceb_insigniaBasic Knowledge

Mechanism of Hemodynamic Monitoring

The rapidly occurring events (represent mechanical forces) of cardiac chambers and vessels during cardaic cycle require conversion to an electrical signal to be transmitted and subsequently translated into an interpretable, graphic format. The pressure transducer is the essential component that translates the mechanical forces to electrical signals. The transducer may be located at the tip of the catheter (micromanometer) within the chamber or, more commonly, the pressure transducer is outside of the body, and a pressure waveform is transmitted from the catheter tip to the transducer through a column of fluid. These transducers consist of a diaphragm or membrane attached to a strain-gauge-Wheatstone bridge arrangement. When a fluid wave strikes the diaphragm, an electrical current is generated with a magnitude dependent on the strength of the force that deflects the membrane. The output current is amplified and displayed as pressure versus time.

Clinical Art

Pre-operations Before Recording

Old generations of transducers required calibration against a mercury manometer; fortunately, the factory-calibrated, disposable, fluid-filled transducers in clinical use today no longer need this. Table-mounted transducers do require balancing or "zeroing," which refers to the establishment of a reference point for subsequent pressure measurements. The reference or "zero" position should be determined before any measurements are made. By convention, it is defined at the patient's midchest in the anteroposterior dimension at the level of the sternal angle of Louis (fourth intercostal space). This site is an estimation of the location of the right atrium and is also known as the phlebostatic axis. A table-mounted transducer is placed at this level and the stopcock is opened to air (atmospheric pressure) and set to zero by the hemodynamic system. The system is now ready for presure measurements. It is important to emphasize that the pre-operation of the hemodynamic monitor is very important, because if the "zero" level is not properly set and the transducer not appropriately balanced, the hemodynamic data recorded would be misleading, even fatal.

Interpretation of pressure waveforms requires a consistent and systematic approach in Table 2-1. Careful scrutiny of the waveform ensures a high-fidelity recording without over- or under-damping. Each pressure event should be timed with EKG.

Table 2-1 A Systematic Approach to Hemodynamic Interpretation
1.Establish the zero level and balance transducer
2.Confirm the scale of the recording
3.Collect hemodynamics in a systematic method using established protocols
4.Critically assess the pressure waveforms for proper fidelity
5.Carefully time pressure events with the EKG
6.Review the tracings for common artifacts

At present, in the clinical setting, 3 pressure waveforms can be obtained at bedside with invasive hemodynaic monitoring devices (central venous cathether/CVC and pulmonary artery catheter/PAC), including right atrial pressure/Prapulmonary artery pressure/Ppa, and pulmonary artery wedge pressure/Ppw. The pressurewave form is recorded along with a synchronized EKG.

Normal Pressure Waveform

Atrial Pressure

The goal of measuring the atrial pressure is to measure the pressure in the ventricles  at the end of diastole, to idenfify a "filling pressure". The goal for any atrial pressure measurement is to obtain the measurement at the every end of diastole, when the atrial pressure is closest to the ventricular pressure. The normal Pra is 2-8 mm Hg and is characterized by a and v waves and x and y descents. The causes of a, v waves and x, y descents are listed below.

PS: The Rationale Reason for the Formation of Pra waveform

a wave represents the pressure rise within the right atrium due to atrial contraction follows the P wave on the EKG by about 80 msec
descet represents the pressure decay following the a wave and reflect both atrial relaxation and the sudden downward motion of the atrioventricular junction that occurs because of early ventricular systole  
c wave is sometimes observed after the a wave and is due to the sudden motion of the tricuspid annulus toward the right atrium at the onset of ventricular systole the c wave follows the a wave by the same time as the PR interval on the EKG
v wave when the tricuspid valve is closed, the pressure rise responsible for the v wave is due to passive venous filling of the atrium, represent atrial diastole. the peak of the right atrial v wave corresponds with the end of T wave on the surface EKG; the ORS alawys appears before the v wave is produced
y wave is due to rapid emptying of the right atrium when the tricuspid valve opens  

Atrial waveform interpretation in detail

v wave

The atrial pressures initially increase during systole as the contracting ventricles return blood to the atria, refilling the upper chambers. This rise in the atrial pressure is identified as the "v" wave. The upstroke of the v wave is the rise in atrial pressure as a result of atrial filling. Because it is produced as a result of ventricular contraction, its location is relative to the QRS on the EKG. Ejection eventually leads to the return of blood to the atria (left ventricular contraction refills the right atrium and produces the right atrial v wave; right ventricular contraction refills the left atrium and produces the left atrial v wave). Thus, the QRS causes the v wave, however, the QRS always appears before the v wave is produced.


The normal pulmonary artery systolic pressure/Ppas is 15-30 mm Hg, the normal diastolic pressure/Ppad is 4-12 mm Hg, and the mean 9-18 mm Hg. The components pulmonary artery pressure include a rapid rise in pressure, systolic peak, a pressure decay associated with a well-defined dicrotic notch from pulmonic valve closure, and a diastolci trough.

PA and arterial pressure waveforms have similar morphology. Systole begins with the opening of the pulmonic valves. Prior to opening of the pulmonary valve, the pulmonary artery pressure is very low (the pulmonary vascular system does not need a high pressure system to perfuse). As the ventricles contact, they eject blood into the pulmonary artery. This causes an immediate rise in the arterial pressure. As blood enters the great vessels, the pressure rise quickly and steadily, producing a steep vertical rise. Late in systole, the rate of ejection slows as the pressure gradient between the right ventricle and pulmonary artery narrows. Although blood is still moving from the ventricle to the great vessels, the rate of movement is slowed to the point where the pressure begins to decline. This cause the early downslope in the arterial tracing that represents this period of reduced ejection. Like the right atrial v wave, the pulmonary artery systolic wave typically coincides with the T wave of the EKG.

Later, the ventricle begins to relax, causing the ventricular pressure to drop below the pressure in great vessels. This causes the pulmonic valves to close, producing a small rise in the PA pressure, known as the dicrotic notch. Following closure of the semi-lunar valves, the pulmonary artery continues to fall as blood leaves the great vessels to perfuse the tissues and lungs.


The normal mean pulmonary artery wedge pressure/Ppw is obtained when the inflated catheter obstructs forward flow within a branch of the pulmonary artery, creating a static column of blood between the tip of the catheter and the j point in the pulmonary venous bed where it intersects with flowing blood. The Ppw tracing contains the same sequence of waves and descents as the Pra tracing. However, when referenced to the ECG, the waves and descents of the Ppw will be seen later than those of the Pra, because the pressure waves from the left atrium must travel back through the pulmonary vasculature and a longer length of catheter. Therefore, in the Ppw tracing, the a wave usually appears after the QRS complex, and the v wave is seen after the T wave.
screen-shot-2016-10-19-at-2-19-49-pmInterpretation of CVP and PAWP measurements

Correlation to the EKG

The easiest wave to evaluate an atrial tracing is to first locate the v wave. Generally, it will appear immeidately after the peak of T wave on a CVP waveform, however, it will be 80-120 ms after the T wave on a PAWP tracing. You can generally identify the v wave by ruling out other waves. It must be after the peak of the T wave. Once the v wave is identified, the a and c can be determined.

Observe the EKG rhythm. If the patient has a sinus rhythm, an a wave should be present. The a should be in the PR interval for a CVP. It is later in the PAWP, appearing within or even afte QRS. If the patient does not have a P wave, the a wave will be absent. If the P wave is not synchronized to the QRS, very large a wave may be present. These large a waves may appear as one very large wave during a cardiac cycle. The large a waves are called cannon a waves. They are actually exaggerated atrial pressures that occur when the atria contract against a closed AV valve, adding to the pressure that is already being generated due to the c or v wave.

If present, the c wave is generally within the QRS for a CVP. It will be after the QRS for a PAWP.

Where to Measure CVP and PAWP

At the very end of ventricular diastole, the atrial pressure equilibrates with the ventricular pressure, at the very end of ventricular filling. Measurement of the atrial pressure at the end of diastole provides the best opportunity to capture ventricular filling pressure. The location on the atrial pressure wave that best reflects end-diastolic pressure is the point just prior to the c wave. However, c wave is often absent or difficult to find, espeically true in the PAWP waveform, which is subject to considerable movement artifact from right ventricular systole and breathing. If we cannot use the mehtod based on c wave to measure the filling pressure, instead we can use other two ways to capture the filling pressure, where the second method for identification of the end-diastolic pressure is to take the mean of the highest and lowest a wave pressure; and the thrid method is used if the a wave is hard to interpret or absent, that is, the end-diastolic pressure can be estimated by identifying the Z point. Draw a line from the end of the QRS to the atrial tracing. The point where the line intersects with the waveform is the Z line. Note that for a PAWP waveform the Z line should be estimated as 0.08-0.12 seconds to the left of the end of the QRS (Z point is delayed 0.08-0.12 seconds from the QRS on the PAWP).

Respiratory Influences on Hemodynamic Data: Transmural Pressure

The Pra and Ppw are used as surrogates for RV and LV filling pressure (so the preload), but remember that when evaluating the patient's preload the end-diastolic volume of the ventricles should also be included in the interpretation. Here in this section we focus our discussion on the respiratory influecnes on the recorded hemodynamic data. OK, it is the transmural (intravascular minus pleural) pressure that represents the distending pressure for cardiac filling. During normal breathing, Ppl is slightly negative at end-expiration and intrathoracic vascular pressures measured at this point in respiratory cycle provide the best estimate of transmural pressure. Either a strip recording or the cursor method should be used to define the end-expiratory pressure.

One error is the assumption that during mechanical ventilation the lowest point in the pressure tracing reflects end expiration. While this is true during controlled ventilation, inspiratory efforts that trigger mechanical breaths produce a nadir in the pressure tracing. Identification of end expiration in the Ppw tracing is aided by the knowledge that expiration is usually longer than inspiration, two exceptions being marked tachypnea and inverse-ratio ventilation. Identification of end expiration from the pressure tracing should not be difficult when interpreted in relationship to the patient's ventilatory pattern. When confusion occurs, a simultaneous airway pressure tracing may be used.

The Pra and Ppw will overestimate transmural pressure if intrathoracic pressure is positive at end expiration. This can occur from an increase in end-expiratory lung volume due to applied positive end-expiratory pressure (PEEP) or auto-PEEP, or from increased intra-abdominal pressure due to active expiration or intra-abdominal hypertension.

Common Errors and Artifacts

screen-shot-2016-10-20-at-7-58-42-pmMost errors in the collection and interpretation of hemodynamic data are listed in Table 2-2.

Probably the most commonly observed artifacts relate to an improper degree of damping. The over-damped tracing indicates the presence of excessive friction absorbing the force of the pressure wave somewhere in the line from the catheter tip to the transducer. The tracing lacks proper fidelity and appears smooth and rounded because of loss of frequency response. This will result in loss of data and will falsely lower peak pressures. Typically, the dicrotic notch on the aortic or pulmonary artery waveforms is absent, and the right atrial or PAPW waveforms will lack distinct a and v waves.

Under-damping causes overshoot or ring artifact. This artifact typically appears as one or more narrow "spikes" overshooting the true pressure during the systolic pressure rise with similar, negatively directed waves overshooting the true pressure contour during the downstroke. This artifact may lead to overestimation of the peak pressure and underestimation of the pressure nadir. Tiny air bubbles that oscillate rapidly back and forth, transmitting energy back to the transducer, cause this artifact. Flushing the catheter or transducer often corrects this artifact; alternatively, introduction of a filter to the hemodynamic system may be necessary to eliminate this artifact.

Related to overshoot or ring artifact is catheter whip or fling artifact. This artifact is created by acceleration of the fluid within the catheter from rapid catheter motion and is commonly seen with balloon-tipped catheters in hyperdynamic hearts or balloon-tipped catheters placed in the pulmonary artery with extraneous loops. Similar to ring artifact, catheter whip causes overestimation of the systolic pressure and underestimation of the diastolic pressure. This artifact is difficult to remedy; eliminating the extra loops or deflation of the balloon can improve the appearance and limit this artifact.

Catheter malposition creates several interesting artifacts.

Acid-Base Disorder Analysis

October 8, 2015 Critical Care, Nephrology, Respirology No comments , , , , , , , ,

Heart attack and sudden cardiac arrestManaging ICU patients without a working knowledge of acid-base disorders is like trying to clap your hands when you have none. In fall of 2015, the first board certification for critical care pharmacist would start and those pass the certification will be addressed with the title of BCCCP, which means the Board Certified Critical Care Pharmacist (Detail here

PS: Blood oxygen partial pressure and oxyhemoglobin saturation

250 mm Hg —> 100%

100 mm Hg —> 97.4%, oxygen content 19.88 mL (chemically bound plus physically dissolved, [Hb] = 15 g/dL)

60 mm Hg —> 90%

40 mm Hg —> 75%, oxygen content 15.2 mL (chemically bound plus physically dissolved, [Hb] = 15 g/dL)

27 mm Hg —> 50%

20 mm Hg —> 32%

Classification of Acid-Base Disorders

According to traditional concepts of acid-base physiology, the [H+] in extracellular fluid is determined by the balance between the partial pressure of carbon dioxide (PCO2) and the concentration of bicarbonate (HCO3) in the fluid. This relationship is expressed as follows:

[H+] = 24 X (PCO2/HCO3) [Equation 1]

The PCO2/HCO3 ratio identifies the primary acid-base disorders and secondary responses. According to equation 1, a change in either the PCO2 or the HCO3 will cause a change in the [H+] of extracellular fluid. When a change in PCO2 is responsible for a change in [H+], the condition is called a respiratory acidosis, and a decrease in PCO2 is a respiratory alkalosisWhen a change in HCO3 is responsible for a change in [H+], the condition is called a metabolic acid-base disorder: a decrease in HCO3 is a metabolic acidosis, and an increase in HCO3 is a metabolic alkalosis.

Secondary responses are designed to limit the change in [H+] produced by the primary acid-base disorder, and this is accomplished by changing the other component of the PaCO2/HCO3 ratio in the same direction. For example, if the primary problem is an increase in PaCO2 (respiratory acidosis), the secondary response will involve an increase in HCO3, and this will limit the change in [H+] produced by the increase in PaCO2. However, secondary responses should not be called “compensatory responses” because they do not completely correct the change in [H+] produced by the primary acid-base disorder.

Responses to Metabolic Acid-Base Disorders

The response to a metabolic acid-base disorder involves a change in minute ventilation that is mediated by peripheral chemoreceptors located in the carotid body at the carotid bifurcation in the neck. The secondary response to metabolic acidosis is an increase in minute ventilation (tidal volume and respiratory rate) and a subsequent decrease in PaCO2. This response appears in 30-120 minutes, and can take 12 to 24 hours to complete. The magnitude of the response is defined by the equation below.

deltaPaCO2 = 1.2 X deltaHCO3 [Equation 2] (metabolic acidosis)

Using a normal PaCO2 of 40 mm Hg and a normal HCO3 of 24 mEq/L, the above equation can be rewritten as follows:

Expected PaCO2 = 40 – [1.2 X (24 – current HCO3)] [Equation 3] (metabolic acidosis)

Example: For a metabolic acidosis with a plasma HCO3 of 14 mEq/L, the deltaHCO3 is 24 -14 = 10 mEq/L, the deltaPaCO2 is 1.2 X 14 = 17 mm Hg, and the expected PaCO2 is 40 – 17 = 23 mm Hg. If the PaCO2 >23 mm Hg, there is a secondary respiratory acidosis. If the PaCO2 is <23 mm Hg, there is a secondary respiratory alkalosis.

The secondary response to metabolic alkalosis is a decrease in minute ventilation and a subsequent increase PaCO2. This response is not as vigorous as the response to metabolic acidosis because the peripheral chemoreceptors are not very active under normal conditions, so they are easier to stimulate than inhibit. The magnitude of the response to metabolic alkalosis is defined by the equation below

deltaPaCO2 = 0.7 X deltaHCO3 [Equation 4] (metabolic alkalosis)

Using a normal PaCO2 of 40 mm Hg and a normal HCO3 of 24 mEq/L, the above equation can be written as follows:

Expected PaCO2 = 40 + [0.7 X (Current HCO3 -24)] [Equation 5] (metabolic alkalosis)

Example: For a metabolic alkalosis with a plasma HCO3 of 40 mEq/L, the deltaHCO is 40 – 24 = 16 mEq/L, the deltaPaCO2 is 0.7 X 16 = 11 mm Hg, and the expected PaCO2 is 40 + 11 = 51 mm Hg. This is only a borderline election in PaCO2, and it demonstrates the relative weakness of the response to metabolic alkalosis.

Responses to Respiratory Acid-Base Disorders

The secondary response to changes in PaCO2 occurs in the kidneys, where HCO3 absorption in the proximal tubes is adjusted to produce the appropriate change in plasma HCO3. This renal response is relatively slow, and can take 2 or 3 days to reach completion. Because of the delay in the secondary response, respiratory acid-base disorders are separated into acute and chronic disorders. Acute changes in PaCO2 have a small effect on the plasma HCO3, as indicated in the following two equations.

For acute respiratory acidosis:

deltaHCO3 = 0.1 X deltaPaCO2 [Equation 6]

Expected HCO3 = 24 + [0.1 X (Current PaCO2 – 40)] [Equation 6.1] (acute respiratory acidosis)

For acute respiratory alkalosis:

deltaHCO3 = 0.2 X deltaPaCO2 [Equation 7]

Expected HCO3 = 24 – [0.2 X (40 – Current PaCO2)] [Equation 7.1] (acute respiratory alkalosis)

Example: For an acute increase in PaCO2 to 60 mm Hg, the deltaHCO3 is 0.1 X (60 – 40) = 2 mEq/L for an acute respiratory acidosis, which would be recognized as non-significant.

For chronic respiratory acidosis, and chronic respiratory alkalosis, respectively

deltaHCO3 = 0.35 X deltaPaCO2 [Equation 8]

Expected HCO3 = 24 + [0.35 X (Current PaCO2 – 40)] [Equation 8.1] (chronic respiratory acidosis)

deltaHCO3 = 0.4 X deltaPaCO2 [Equation 9]

Expected HCO3 = 24 – [0.4 X (40 – Current PaCO2)] [Equation 9.1] (chronic respiratory alkalosis)

Example: For an increase in PaCO2 to 60 mm Hg that persist for at least a few days, the deltaPaCO2 is 60 – 40 = 20 mm Hg, the deltaHCO3 is 0.35 X 20 = 7 mEq/L, and the expected HCO3 is 24 + 7 = 31 mEq/L.

Stepwise Approach to Acid-Base Analysis

Stage I: Identify the primary acid-base disorder. In the first stage of the approach, the PaCO2 and pH are used to identify the primary acid-base disorder.

Rule 1: If the PaCO2 and/or the pH is outside the normal range, there is an acid-base disorder.

Rule 2: If the PaCO2 and pH are both abnormal, compare the directional change, where if the PaCO2 and pH change in the same direction, there is a primary metabolic acid-base disorder and if the PaCO2 and pH change in opposite directions, there is a primary respiratory acid-base disorder.

Rule 3: If only the pH or PaCO2 is abnormal, the condition is a mixed metabolic and respiratory disorder. If the PaCO2 is abnormal, the directional change in PaCO2 identifies the type of respiratory disorder and the opposing metabolic disorder. If the pH is abnormal, the directional change in pH identify the type of metabolic disorder and the opposing respiratory disorder.

PS: Reference ranges for arterial pH, PCO2, and HCO3 pH = 7.36 – 7.44 PCO2 = 36 – 44 mm Hg HCO3 = 22 – 26 mEq/L

Stage II: Evaluate the secondary responses. The secondary stage of the approach is for cases where a primary acid-base disorder has been identified in Stage I. (If a mixed acid-base disorder was identify in Stage I, go directly to Stage III). The goal in stage II is to determine if there is an additional acid-base disorder.

Rule 4: For a primary metabolic disorder, if the measured PaCO2 is higher than expected, there is a secondary respiratory acidosis, and if the measured PaCO2 is less than expected, there is a secondary respiratory alkalosis.

Example: Consider a case where the PaCO2 = 23 mm Hg, the pH = 7.32, and the HCO3 = 16 mEq/L. The pH and PaCO2 change in the same direction, indicating a primary metabolic disorder, and the pH is academic, so the disorder is a primary metabolic acidosis. The expected expected PaCO2 = 40 – [1.2 X(24 – 16)] = 30 mm Hg. So the current PaCO2 (23 mm Hg) < expected PaCO2 (30 mm Hg), and there is a secondary respiratory alkalosis.

Rule 5: For a primary respiratory disorder, a normal or near-normal HCO3 indicates that the disorder is acute.

How to distinguish acute and chronic respiratory disorder?

First we should focus on the clinical situation of the patient, including patient history, physical exam, and laboratory findings.

For acute respiratory acidosis, (delta pH)/(delta PaCO2) = approximately 0.008; for chronic respiratory acidosis, (delta pH)/(delta PaCO2) = approximately 0.003.

For acute respiratory alkalosis, (delta pH)/(delta PaCO2) = approximately 0.008; for chronic respiratory alkalosis, (delta pH)/(delta PaCO2) = approximately 0.003.

Rule 6: For a primary respiratory disorder where the HCO3 is abnormal, determine the expected HCO3 for a chronic respiratory disorder. For a chronic respiratory acidosis, if the HCO3 is lower than expected, there is an incomplete renal response, and if the HCO3 is higher than expected, there is a secondary metabolic alkalosis. For a chronic respiratory alkalosis, if the HCO3 is higher than expected, there is an incomplete renal response, and if the HCO3 is lower than expected, there is a secondary metabolic acidosis.

Example: Consider a case where the PaCO2 = 23 mm Hg, the pH = 7.54, and the HCO3 = 38 mEq/L. The PaCO2 and pH change in opposite directions, indicating a primary respiratory disorder, and the pH is alkaline, so the disorder is a primary respiratory alkalosis. The HCO3 is abnormal, indicating that this is not an acute respiratory alkalosis. The expected HCO3 = 24 – 0.4 X (40 – 23) = 17 mEq/L. So the patient also has metabolic alkalosis.

Stage III: Use the “Gaps” to evaluate a metabolic acidosis. The final stage of this approach is for patients with a metabolic acidosis, where the use of measurements called gaps can hep to uncover the underlying cause of the acidosis. Anion Gap The anion gap is a rough estimate of the relative abundance of unmeasured anions, and is used to determine if a metabolic acidosis is due to an accumulation of non-volatile acids or a primary loss of bicarbonate.

AG = Na – (Cl + HCO3) [Equation 9]

Reference range is 8 to 16 mEq/L The AG can be used to identify the underlying mechanism of a metabolic acidosis, which then helps to identify the underlying clinical condition. An elevated AG occurs when there is an accumulation of fixed or non-volatile acids (e.g., lactic acidosis), while a normal AG occurs when there is a primary loss of bicarbonate (e.g., diarrhea).

The anion gap should always be adjusted for the albumin concentration, because this weak acid may account for up to 75% of the anion gap. Without correction for hypoalbuminemia, the estimated anion gap does not reveal a clinically significant increase in anions (>5 mmol per liter) in more than 50% of cases. Generally, for every decrement of 1 g per deciliter in the serum albumin concentration, the calculated anion gap should be increased by approximately 2.3 to 2.5 mmol per liter. However, the albumin-corrected anion gap is merely an approximation, since it does not account for ions such as magnesium, calcium, and phosphate ions.

High AG: Common causes of high AG metabolic acidosis are lactic acidosis, diabetic ketoacidosis, and advanced renal failure (where there is loss of H+ secretion in the distal tubules of the kidneys). Also included are toxic ingestions of methanol (which produces formic acid), ethylene glycol (which produces oxalic acid), and salicylates (which produce salicylic acid).

Normal AG: Common causes of a normal AG metabolic acidosis are diarrhea, saline infusion, and early renal failure (where there is loss of bicarbonate reabsorption in the proximal tubules). The loss of HCO3 is counterbalanced by a gain of chloride ions to maintain electrical charge neutrality; hence the term hyperchloremic metabolic acidosis is used for normal AG metabolic acidoses (In high AG metabolic acidoses, the remaining anions from the dissociated acids balance the loss of HCO3, so there is no associated hyperchloremia).

The Gap-Gap Ratio

In the presence of a high AG metabolic acidosis, it is possible to detect another metabolic acid-base disorder (a normal AG metabolic acidosis or a metabolic alkalosis) by comparing the AG excess (the difference between the measured and normal AG) to the HCO3 deficit (the difference between the measured and normal HCO3 in plasma). This ratio is sometimes called the gap-gap ratio because it involves two gaps.

Mixed Metabolic Acidoses In metabolic acidoses caused by non-volatile acids (high AG metabolic acidosis), the decrease in serum HCO3 is equivalent to the increase in AG, and the gap-gap ratio is unity or 1. However, if there is a second acidosis that has a normal AG, the decrease in HCO3 is greater than the increase in AG, and the gap-gap ratio falls below unity (<1). Therefore, in the presence of a high AG metabolic acidosis, a gap-gap ratio <1 indicates the coexistence of a normal AG (hyperchloremic) metabolic acidosis.

Updated on Dec 16 2015

The Delta Ratio (∆/∆)

The delta ratio is sometimes used in the assessment of elevated anion gap metabolic acidosis to determine if a mixed acid base disorder is present. 

Delta ratio = ∆ Anion gap/∆ [HCO3-] or ↑anion gap/  [HCO3-]  

Delta Delta =  Measured anion gap – Normal anion gap

Delta del = Normal [HCO3-] – Measured [HCO3-]

Delta Delta/Delta del = (AG – 12) / (24 – [HCO3-])

In order to understand this, let us re-examine the concept of the anion gap.

If one molecule of metabolic acid (HA) is added to the ECF and dissociates, the one H+ released will react with one molecule of HCO3- to produce CO2 and H2O. This is the process of buffering. The net effect will be an increase in unmeasured anions by the one acid anion A- (ie anion gap increases by one) and a decrease in the bicarbonate by one meq.

Now, if all the acid dissociated in the ECF and all the buffering was by bicarbonate, then the increase in the AG should be equal to the decrease in bicarbonate so the ratio between these two changes (which we call the delta ratio) should be equal to one. 

As described previously, more than 50% of excess acid is buffered intracellularly and by bone, not by HCO3- . In contrast, most of the excess anions remain in the ECF, because anions cannot easily cross the lipid bilayer of the cell membrane. As a result, the elevation in the anion gap usually exceeds the fall in the plasma [HCO3- ].  In lactic acidosis, for example, the ∆/∆ ratio averages 1.6:1

On the other hand, although the same principle applies to ketoacidosis, the ratio is usually close to 1:1 in this disorder because the loss of ketoacids anions (ketones) lowers the anion gap and tends to balance the effect of intracellular buffering. Anion loss in the urine is much less prominent in lactic acidosis because the associated state of marked tissue hypoperfusion usually results in little or no urine output.

Screen Shot 2015-12-16 at 1.02.52 PM

A delta-delta value below 1:1 indicates a greater fall in [HCO3-] than one would expect given the increase in the anion gap. This can be explained by a mixed metabolic acidosis, i.e a combined elevated anion gap acidosis and a normal anion gap acidosis, as might occur when lactic acidosis is superimposed on severe diarrhea. In this situation, the additional fall in HCO3- is due to further buffering of an acid that does not contribute to the anion gap. (i.e addition of HCl to the body as a result of diarrhea)

A value above 2:1 indicates a lesser fall in [HCO3-] than one would expect given the change in the anion gap. This can be explained by another process that increases the [HCO3-],i.e. a concurrent metabolic alkalosis. Another situation to consider is a pre-existing high HCO3- level as would be seen in chronic respiratory acidosis.

Updated on Sep 9th 16

Blood Gas Variability

screen-shot-2016-09-09-at-1-28-47-pmThe arterial PO2 and PCO2 can vary spontaneously without a change in the clinical condition of the patient. This is demonstrated in Table 20.2, which shows the spontaneous variation in arterial PO2 and PCO2 over a one-hour period in a group of clinical stable trauma victims. Note that the arterial PO2 varied by as much as 36 mm Hg, while the arterial PCO2 varied by as much as 12 mm Hg. This variability has also been observed in patients in medical ICU. Because this degree of spontaneous variation, routine monitoring of arterial blood gases can be misleading.