Arterial Blood Gas Analysis

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In this session we will discuss in detail how to make and, subsequently, how to interpret arterial blood gas sample.

ABG sampling – How to

  • ABG sample from radial artery
  • ABG sample from brachial artery
  • ABG sample from femoral artery
  • Ultrasound-guided ABG

Radial ABG sampling

Arterial puncture, as many of you know, can sometimes generate a little anxiety as it’s seen as a painful procedure. Actually if done properly, it will cause the patient a pain very similar, if not lower, to a venous withdrawal.
Let’s examine in detail the technique of execution.
The most important part is the palpation of the arterial pulse that must meet certain parameters:
1 ) The fingers must be placed perpendicular to the skin , like an “hammer” to reduce skin contact surface and better localize radial pulsation.
2 ) When you lean the fingers on the pulse of the patient feels almost always a pulsation (unless the patient is hypotensive ) but is getting a little ‘hard to figure out where exactly sting . To understand the right point you have to find the ” point of maximum pulse ” of the artery . To do this you need to lift your fingers and move ” back and forth ” like in the movie to make disappear the pulsation of the artery first one way and then the other. This way you will be able to find more clearly the point where the artery ” pulsates more” and you will be ready to sting . For better accuracy of the point of insertion of the needle you can place the ” point of maximum pulse ” between the finger and the nail.

Now you are ready to take the next step, take the syringe.
It’s important to remember that the most delicate phase of the ABG sampling resides in the wrist palpation to find the point of maximum pulsatility of radial artery. Take all the time you need to palpate and a half seconds to sting. Performing a blind puncture, hoping for a miracle of “ABG-God”, generally does not bring good results, in particular with regard to the patient’s pain. You have to insert needle in the proximal portion of the wrist, possibly no more than 3-4 cm from the crease of the hand. This is because at this point the artery passes through two ligaments of the wrist, the palmar ligament and the transverse carpal ligament, becoming less “mobile” and “slippery”
polso
Place the needle at 45° (or 20-30° if you taste a very superficial artery eg. in elderly or cachectic) and insert it quickly to reduce pain.
To stay on this last topic, avoid telling the patient you’re going to hurt him: to anticipate the pain generates anxiety and amplifies the painful sensation. Inform you patient you are going to perform an arterial puncture, just as you do before a venipuncture.
The pain is usually caused by repeated attempts to puncture through the tendons of the forearm muscles (the tendon of the flexor carpi and the tendon of the long flexor of the thumb).

 

Brachial ABG

Why make a withdrawal from the brachial artery? Those of you who already tried to perform a radial ABG, or even those who have seen do it, will know that sometimes the arterial pulse may not be palpable. Reasons, unless being in front of a patient in cardiopulmonary arrest of course, can be different: hypotension, excessive depth of the vessel, big wrist, and so on.
In these situations, brachial artery is to prefer, ibecause of its bigger calibre.
Where must we puncture? At the level of the elbow crease, in its medial portion.
Courtesy of Netter Atlas
Courtesy of Netter Atlas

 

The technique of execution is different than the radial drawing, because brachial artery is more mobile. The first thing to do is to isolate it between the index and middle fingers of the left hand. Next thing to do is to find the point of maximum pulsatility with the index and/or middle of the other hand. Found the point of maximum pulse puncturing the artery with the needle perpendicular to the skin.

 

Femoral ABG

Arterial blood gasanalysis sampling, performed at the level of the femoral artery is, despite initial fears, easier to do and less painful for the patient. Given the depth of the femoral artery, it’s a good practice to replace the needle of the syringe native with a longer one.
Femoral artery is also useful, in addition to the arterial puncture, even for a simultaneous withdrawal of common blood tests, using a small extension tube, a three-way and a vacutainer.
2012-09-08 14.51.59
Where to insert the needle? Along the medial aspect of the inguinal crease.
Femoral_Artery
The technique is the same used for brachial ABG (see video). You have to isolate the artery between the index and middle fingers of the left hand, and find the point of maximum pulse with the index and / or middle fingers of the right hand. Once you find it, you have to insert the needle perpendicular to the skin.
It’s important to remember to perform a compression after collection for at least one minute (increase to 3-5 minutes in case of anticoagulant theraphy) to avoid complications.

Ultrasound-guided ABG

The technique is the same at the level of both sampling sites, brachial or femoral. Generally linear probe is the most performing tool but in case of necessity you can also use a convex probe or phased array (in these cases collecting sample may be more difficult in relation to the lower resolution of the probes). The probe is placed perpendicular to the skin placing the vessel in the center of the monitor.
The middle of the probe is thus used as a landmark for needle insertion.
Then you have to puncture in the vicinity of the probe slightly inclined (about 70-80 °) to make sure that the tip of the needle, after the puncture of the skin, head below the probe and can be viewed in the monitor. When the needle reaches the vessel is displayed on the monitor as a small spot hyperechoic (white) within it.
Complications of ABG
 
The most common complication is pain, but using a proper technique and with a little experience, sampling arterial become painful as a venipuncture or less. The pain is in fact is caused by repeated attempts to find the artery, and is accentuated by the hit of muscle tendons.
The vaso-vagal crisis is the second complication for frequency and affects predisposed subjects; typically occurs after the puncture. The patient complains of malaise and looks pale and sweating. Heart rate and blood pressure decreases and loss of consciousness may occur. In most cases it is sufficient to put the patient supine, lifting the lower limbs to facilitate the venous return but in some cases intravenous administration of atropine (0.5 mg / repeatable) may be necessessary.
The most feared complication is represented by iatrogenic pseudoaneurysm that occurs as a result of perivascular leakage of blood from the through hole caused by the needle, after its removal. Iatrogenic pseudoaneurysm occurs mostly in patients receiving anticoagulant therapy. In this kind of patients  a correct and prolonged compression is mandatory.

ABG Interpretation

There are several approaches to the interpretation of ABG.
The classic method involves comparison between bicarbonate and carbon dioxide in order to understand pH variations. There is, however, another method (named Stewart’s), that considers the difference between strong ions (SID – Strong Ion Difference) and weak acids (Atot – Total Weak Acid) to interpret pH changes.
In this session we will use the classical method, simple and versatile, though less fascinating.
In this webpage we’re going to utilize IRC-ALS method (Advanced Life Support of Italian Resuscitation Council) which provides a five-step approach modified (I’ve added a 6 ° step):
1) Assess the patient
2) Assess oxygenation (pO2)
3) Evaluate the pH
4) Evaluate the carbon dioxide (pCO2)
5) Evaluate the bicarbonate (HCO 3)
6) Evaluate the compensation expected (simple and complex disorders)
1) Assess the patient
The clinical condition of the patient and the medical history data are the first things to consider before you engage in ABG-diagnosis. The presence of chronic respiratory acidosis (COPD) and/or the presence of conditions that are associated with chronic respiratory alkalosis (eg. pregnancy or cirrhosis) are necessary elements in order to calculate the correct acid-base disorder. Furthermore knowledge patient’s clinical history also helps in the diagnosis. For example, a patient who has undergone a cardiopulmonary arrest will have a high probability of having lactic acidosis, while a excessively-ventilated patient may present a iatrogenic respiratory alkalosis.
2) Assess oxygenation
 
The pO2 value is the second data to be evaluated since a hypoxemic patient will develop complications very quickly. The pO2 value should always be compared with the percentage of oxygen that the patient is breathing (P/F ratio).
For example let’s consider the following ABG in three different types of patients:
pH = 7,45 (vn 7,35 – 7,45)
pO2 = 85 mmHg (vn > 60)
pCO2 =  37 mmHg (vn 35-45)
HCO3 = 23 mmol/l (vn 22-26)
SaO2 = 95%
Patient A: 24 year old, male, who shows up for sensation of dyspnea. In history no significant pathology, does not take drugs, no drug allergy. Presents a recent stressful period (university exams). ABG was performed in ambient air (FiO2 = 21%).
Patient B: 78 year old, female, came to the emergency department for fever and cough for several days. During ABG sample she breathed oxygen in ventimask 35%.
Patient C: 32 year old boy with severe polytrauma (thrown 30ft from his motorcycle). The ABG sample is carried out while patient was breathing in oxygen mask with reservoir bag (FiO2 = 85%).
P/F values are different in the three patients above, even though ABG is the same:
A) pO2 = 85 mmHg, FiO2 = 21% (ambient air). P / F = 85 / 0.21 = 404 (normal)
B) pO2 = 85 mmHg, FiO2 = 35%. P / F = 85/0.35 = 242 (moderate respiratory failure)
C) pO2 = 85 mmHg, FiO2 = 85%. P / F = 85 / 0.85 = 100 (severe respiratory failure)
3) Evaluate pH values
 
Normal values of pH are between 7.35 and 7.45 and reflect the concentration of acids [H +] in the blood. Maintaining pH within these values is essential for normal homeostasis of the body. The human body functions best at a pH of 7.40-7.42. Human proteins, hence cellular function, have reduced bioactivity at a pH outside of this value. Anything less than 7.35 is an acidosis. Anything above 7.45 is an alkalosis
The pH value depends on the concentration of pO2 and HCO3 as can be deduced from the equation of Henderson-Hasselbalch:
                           [HCO3-]
pH = 6,1 +  ————–
k x [pCO2]
k: pCO2 solubility coefficient
The higher the value of HCO3- (numerator) the higher the pH (alkalosis), while the highest value of pCO2 (denominator), the lower the pH (acidosis). For the same reasons mathematicians, low values of HCO3- cause acidosis, while low values of pCO2 determine alkalosis.
Values of pH tell us a lot about the condition of the patient. The more the pH values deviates from the norm, the more the conditions of the patient are critical.
 
4) Evaluate pCO2 values
 
The carbon dioxide is the end product of tissue catabolism. From tissues carbon dioxide is transported inside red blood cells to lungs and here is eliminated by breathing. The removal of the CO2 produced is therefore dependent on the ability of the blood to reach the lung tissue (cardiac output) and the ability of the lung to eliminate carbon dioxide (diffusion and ventilation).
If there is an accumulation of pCO2, for example due to a decrease of pulmonary ventilation, occurs acidosis while in the opposite case occurs alkalosis. As the primary system of such alteration is the lung, it is called respiratory acidosis or alkalosis.
We try to better understand why an accumulation of pCO2 causes acidosis while excessive elimination determines alkalosis.
To do this we need to know the equation that governs the bicarbonate buffer system:
 H20 + CO2  = [H+] + [HCO3-]
If pCO2 value increases, i.e. due to patient hypoventilation, the balance of the formula will shift to right with increased production of both H + and HCO3- in the same quantity (equimolar). The more astute of you will ask: “Very good, then how can patient develop acidosis since HCO3 and CO2 are formed in equal measure?”. This is due to the fact that the concentration of HCO3- ions is 1000000 times higher than that of H + ions.
The increase will take place in this proportion (simplification):
                              [H+]      [HCO3-]
+1 CO2             1           1000001
+2 CO2             2           1000002
+3 CO2             3           1000003
+4 CO2             4           1000004
+5 CO2             5           1000005
Thus if CO2 values increase by 3-fold then H+ concentration will become 3-fold bigger while concentration of HCO3 will increase only a little bit. The end result is an acidosis. Conversely a decrease of the CO2 will cause alkalosis with reverse mechanism.
Facing with an ABG, the first thing to do is undrestand if pH disorder is due to an alteration of the values of pCO2, in other words we need to understand if the primary disorder is respiratory or not:
– If pH  is less than 7.35 (acidosis) and the values of pCO2 are high (> 45 mmHg) we are dealing with respiratory acidosis: the primary disorder that caused the decrease in pH is increased CO2.
– If pH is more than 7.45 (alkalosis) and the values of pCO2 are low (<35 mmHg) we are dealing with respiratory alkalosis: the primary disorder that caused the increase in pH is the decrease of CO2.
If one of two conditions above is true and then you have done diagnosis of respiratory acidosis or alkalosis, you can skip step 5 and go to step 6.
On the contrary go to step 5.
 
5) Evaluate HCO3
 
Bicarbonate is the major buffer system of the organism. The task of a buffer is to minimize the changes in [H +]. The major source of [H +] is rapresented by  catabolism of foods.
Foods –> [H+] + HCO3– –> CO2 + H20 (Lung)
                                |—— > Kidney
Buffer systems are very effective, for a while, to remove the [H +] body. To make a buffer system efficient it must be present in large amounts and it must be regenerable. HCO3 has both of these features.
If the excess of [H +] is not eliminated by the buffer systems, binds with the proteins of the organism causing an alteration of their morphology and thus their functions. This process sooner or later will leads to cells death.
– If pH is less than 7.35 (acidosis) and the values of HCO3- are low (<22 mEq / l) we are dealing with metabolic acidosis: the primary disorder is a loss of bicarbonate (eg. diarrhea) or an increase of acids consuming bicarbonate buffer system (eg. diabetic ketoacidosis).
– If pH is more than 7.45 (alkalosis) and the values of HCO3- are high (> 26 mEq / l) we are dealing with metabolic alkalosis: the primary disorder is an increase of bicarbonate (ie. iatrogenic) or in a loss of acids (eg. vomiting).
6) Evaluate the compensation expected (simple and complex disorders)
 
At this point you should be able to know if your patient has an acidosis (or alkalosis) respiratory or metabolic and you should know primary disorder. If not so, retrace the steps 1 to 5.
Established the primary disorder is necessary to calculate the compensation expected. For each alteration of acid-base, in fact, the body responds with a compensation in the opposite direction to maintain the neutrality of the pH required for proper cell function and the degree of compensation can be calculated using simple mathematical formulas.
We have a simple disorder if compensation is respected (ed. acute respiratory acidosis), otherwise we will be faced with a complex disorder (ed. acute overlying chronic respiratory acidosis, or metabolic acidosis associated with respiratory acidosis). Let’s see how to calculate compensation in the various primary disorders.
In case of respiratory acidosis, a disorder characterized by increased pCO2, the body reacts by regenerating a larger quantity of bicarbonate in the kidney. This mechanism starts as soon as the pH drops below the optimal values but takes several days to be fully activated. The expected increase of HCO3 is 1 mmol/L for each increment of 10 mmHg pCO2 in the acute disorder and 3.5 mEq / L for each increment of 10 mmHg pCO2 in chronic disorder (ie if respiratory acidosis persists more than 2-3 days).
Respiratory acidosis occur when there is an accumulation of pCO2 and this can happen for any respiratory system problem:
1. CENTRAL: Drugs (anesthetics, morphine, sedatives), Stroke, Infections
2. AIRWAYS: Obstruction (Asthma, COPD)
3. PARENCHYMA: Emphysema, Pneumoconiosis, Bronchitis, dult respiratory distress syndrome, Barotrauma
4. NEUROMUSCOLAR: Poliomyelitis, Kyphoscoliosis, Myasthenia, Muscular dystrophies
5. PARIETAL: PNX, massive pleural effusion
In case of respiratory alkalosis, a disorder characterized by a decrease in pCO2, the body reacts by removing bicarbonate in the kidney. This mechanism starts as soon as the pH rises above the optimum values but takes several days to be activated to the maximum. The expected decline for HCO3 is 2 mmol/L for every decrease of 10 mmHg pCO2 in the acute phase and 5 mmol/ L for every decrease of 10 mmHg pCO2 in chronic phase (ie, if the respiratory alkalosis persists more than 2-3 days).
Respiratory alkalosis occurs when there is a decrease of pCO2 and this happens in each case of hyperventilation:
1. CENTRAL NERVOUS SYSTEM STIMULATION: Pain, Anxiety, Psychosis, Fever, Cerebrovascular accident, Meningitis, Encephalitis, Tumor, Trauma
2. HYPOXIEMIA: High altitude, Low PaCO2, Pneumonia, Pulmonary edema, Aspiration, Severe anemia
3. DRUG OR HORMONES: Pregnancy/High Progesterone, Salcylates intoxication
4. STIMULATION OF CHEST RECEPTORS: Hemothorax, Flail chest, Cardiac failure, Pulmonary embolism
5. MISCELLANEOUS: Septicemia, Hepatic failure, Mechanical hyperventilation, Heat exposure, Recovery from metabolic acidosis
In case of metabolic acidosis, a disorder characterized by an increase in the concentration of [H +] or by a loss of HCO3, the body reacts by eliminating volatile acids, ie pCO2, by increasing the ventilation. This mechanism is activated rapidly and continues over time until fatigue onset in respiratory muscles. It’s not provided a chronic phase of the compensation, as it happens in the kidney. The expected decline of pCO2 of 1.2 mm Hg for each decrement of 1 mmol/l HCO3.
To understand if acidosis is caused by an increase in acid production or by a loss of bicarbonates we hato to introduce the concept of anion gap (AG).
Anion gap literally means “anion deficit”, namely deficit of ions with a net negative charge.  In our body, positive charge ions (cations) must be equal to the negative charge ions (anions) to maintain electroneutrality. The main positive charge ions are given by the sodium (Na +) and potassium (K +), while the main negative charges are given by chlorine (Cl-) and bicarbonate (HCO3-).
However the result of subtraction betweeen anions and cations is not zero, as one might expect:
AG = Cations – Anions = (Na + K) – (Cl + HCO3) = (140 + 4) – (104 + 25) = 15 (vn <12-16)
(some authors prefer not to consider potassium, in this case consider the normal value of AG = 12)
The value of AG represents the quantity of serum unmeasured anions (protein, sulfates, phosphates).
If acidosis is caused by an increase in the acid quantity, the acid added dissociates in [H +] and its corresponding anion [A-]. The hydrogen ion reacts with bicarbonate buffer [HCO3] while the anion [A-] takes its place thus ensuring electroneutrality.
A practical example is given by lactic acidosis:
Hypoxia -> Lactic Acid = [H +] + [lactate] -> HCO3 + [H +] + [lactate] = H2O + CO2 + [lactate]
Assume that we add an amount of lactate able to reduce HCO3 from 25 mmol/l (normal value) to 15 mmol/l.
The reduction of HCO3 will manifest itself in the equation of the calculation of the AG:
AG = Cations – Anions = (Na + K) – (Cl + HCO3) = (140 + 4) – (104 + 15) = 25 (vn <12-16)
Anion gap metabolic acidosis is caused by the body producing too much acid:
– Ketoacidosis (diabetic, alcoholic, fasting)
– Lactic acidosis
– Renal failure
– Intoxication (methanol, ethylene glycol, salicylates, paraldehyde)
If metabolic acidosis is caused by a loss of bicarbonate the kidney will increase the resorption of chlorine (Cl-) so as to maintain electroneutrality. Suppose a loss of 10 mmol/l of bicarbonate: the kidney reacts reabsorbing about 10 mg/dl of chlorine to ensure electroneutrality.
Let’s see what happens in the equation of the calculation of AG.
AG = Cations – Anions = (Na + K) – (Cl + HCO3) = (140 + 4) – (114 + 15) = 15 (vn <12-16)
Non-gap metabolic acidosis (or hyperchloraemic) is due to a loss of bicarbonates:
– Loss of HCO3 gastrointestinal (diarrhea, ureteroenterostomia, pancreatic fistula)
– Loss of renal HCO3 (renal tubular acidosis, hyperparathyroidism, carbonic anhydrase inhibitors)
– Hypoaldosteronism
– Administration of large amounts of Saline Solution ev (NaCl 0,9%): the increase of chlorine causes bicarbonate loss to ensure electroneutrality.
In case of metabolic alkalosis, disorder characterized by a loss of [H +] or by an increase of HCO3, the body reacts by holding volatile acids, ie pCO2, through a decrease in ventilation. Metabolic disorders do not have a chronic phase of the compensation, as happens in the respiratory disorders.
The metabolic alkalosis is due to:
– Load of bicarbonate (milk-alkali syndrome, administration of HCO3 ev)
– ECV (Effective Circulating Volume) reduced: vomiting, SNG, villous adenoma, diuretics, were edematous
– ECV increased: hyperaldosteronism, Cushing, licorice
– Genetic causes (Liddle, Bartter, Gitelman)
N.B. Compensation cannot entirely normalize the pH value! The presence of normal pH should suggest the presence of mixed disorder.
Let’s now try to put into practice what we have learned.
Case #1
A Man, about 30 years fo age, was found unconscious in a park. Near the patient was detected a tourniquet and a syringe. Objectively there are multiple signs of venipuncture in both arms. No signs of trauma. BP 90/60. HR (heart rate): 65 / min. RR (respiratory rate): 7 / min. SaO2 94% (Reservoir FiO2 85%). GCS 10/15 (e2v2m5).
Step 1: How is the patient? 
The patient is in coma, probably due to overdose of opiates. Can not be excluded other substances of abuse (alcohol, benzodiazepines, other). There are no signs of trauma. The cardiac and respiratory function are depressed. We expect low pO2 values and high values of pCO2 due to central hypoventilation secondary to opiate intoxication.
We performe an ABG in emergency room:
pH = 7.22
pO2 = 85 mmHg
PCO2 = 70 mmHg
HCO3 = 28 mEq / l
SaO2 = 94%
FiO2 = 85% (reservoir)
Step 2: Evaluate pO2
At first glance both pO2 value and pulsossimetry seem normal. In fact the patient is breathing high-flow oxygen and to detect the presence of respiratory failure you must calculate the P/F ratio (PaO2/FiO2).
P / F = 85 / 0.85 = 100 (vn> 300) is a severe respiratory failure that must be resolved quickly.
Step 3: Evaluate the pH
pH is <7.35: there is acidosis
Step 4: Evaluate the pCO2
We found an increase in the values of pCO2 as the value returned was > 45 mmHg. The primary disorder is a respiratory acidosis. Skip to step 6.
Step 5: Evaluate the values of HCO3
It’s not necessary at the moment as you have already found the primary cause of the disorder.
Step 6: Assess the expected compensation
The pCO2 is increased by 30 mmHg compared to the normal value (70-40 = 30). We expect an increase of 1 mmol/l x 3 = 3 mEq / L of HCO3 (compared to its normal value using as reference of 25 mEq / L) in case of acute disorder as the pCO2 increased by 3 times 10. We expect a increase of 3.5 mmol/l x 3 = 10.5 mEq / l if the disorder is chronic.
HCO3 expected value in acute: 25 + 3 = 28 mmol/l
HCO3 expected value in chronic: 25 + 10.5 = 35.5 mmol/l
Comparing this result with our value (28 mEq) we can make diagnosis of simple disorder: ACUTE RESPIRATORY ACIDOSIS.
CLINICAL COURSE: The patient is treated with 0,4 mg of intravenous naloxone and 0,8 mg of naloxone intramuscularly (to ensure a more lasting effect), with full recovery of consciousness and complete normalization of arterial blood gases in about 20 minutes . It wasn’t necessary endotracheal intubation.
Case #2
 
A 78-year-old man with severe COPD in therapy with inhaled bronchodilators and both inhaled and oral steroids. He was admitted to the hospital because of stabbing chest pain that increases with coughing. The patient reported that he fell to the ground 10 days ago with a secundary chest trauma. On examination he referred mild soreness at the level of 5° right rib. BP: 120/80. HR: 70 / bpm. SaO2 91%. RR: 14 / min. The ECG was normal.
 
Step 1: How is the patient? 
The patient had a non cardiac chest pain secondary to fracture/infringement of one o more ribs. The clinical conditions were good, had normal respiratory. Pulsossimetry was in the lower limits in relation to the known COPD. We can expect the signs of a possible analgesic hypoventilation secondary to trauma. Since chest trauma happened 10 days before, the kidney should have already established a good compensation.
An ABG was performed:
pH = 7.31
pO2 = 62 mmHg
PCO2 = 80 mmHg
HCO3 = 39 mEq / l
SaO2 = 91%
 
Step 2: Evaluate pO2
The values of pO2 and pulsossimetry were the lower limits of normal.
The P/F was slightly decreased:
P/F = 62 / 0.21 = 295 (vn> 300)
The patient may benefit from low-flow oxygen.
Step 3: Evaluate pH
The patient was acidotic since pH was lower than 7.35.
 
Step 4: Evaluate pCO2
The patient had pCO2 values increased since the value was > 45 mmHg. The  leading disorder was respiratory acidosis. Let’s skip to step 6.
 
Step 5: Evaluate the values of HCO3
It’s not necessary since you have already found the primary disorder (respiratory acidosis).
 
Step 6: Assessing the compensation
The pCO2 was increased by 40 mmHg compared to its normal value (80-40 = 40).
We expect an increase of 1 mmol/L x 4 = 4 mmol/L of HCO3 compared to its normal value (using as reference 25 mmol/L) in case of acute disorder as the pCO2 increased by 4 times 10. We expect a increase of 3.5 x 4 = 14 mEq / l if the disorder is chronic.
HCO3 expected value in acute disorder: 25 + 4 = 29 mEq
HCO3 expected value in chronic disorder: 25 + 14 = 39 mEq / l
Comparing with our value (39 mEq) we can make diagnosis of simple disorder: CHRONIC RESPIRATORY ACIDOSIS
CLINICAL COURSE
Chest X-Ray was performed which confirmed the clinical suspicion of infringement of the right V rib without pleuro-parenchymal injury. The patient was discharged with analgesic therapy (paracetamol plus tramadol per os).
PRIMARY DISORDER COMPENSATION
Resp. Acid Acute ↑ 10 pCO2 ↑ 1 HCO3
Chronic ↑ 10 pCO2 ↑ 3,5 HCO3
Resp. Alk Acute ¯ 10 pCO2 ¯ 2 HCO3
Chronic ¯ 10 pCO2 ¯ 5 HCO3
Metabolic Acidosis ¯ 1 HCO3 ¯ 1,2 pCO2
Metabolic Alkalosis ↑ 1 HCO3 ↑ 0,5 pCO2
These arguments may initially be difficult to understand and, even after having acquired a complete control, are difficult to remember. For this reason I created a App called ABG Ultimate which calculates the compensation expected and analyzes the blood gases (if you need to focus more on the patient’s clinical condition without losing time). It’s available in English, Spanish, French, German, Italian, Romanian and Russian. It’s available on App Store and Google Play Store (link below).
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