Instructions, Computerlab Acid Base Balance (Syrabas-Balans) (Programversion 041011) 111114 (Translation of Swedish Version 110209)

Karolinska Institutet Advanced Physiology HL 2017 och Advanced Physiology smaller course HL-2018

Institutionen för Medicinsk Biokemi och Biofysik

Instructions, computerlab acid base balance (syrabas-balans) (programversion 041011) 111114 (translation of Swedish version 110209)

The aim with this lab exercise is to practice how to reason about medical acid base, and to become acquainted with the Siggaard-Andersen (SA) terminology and nomogram for diagnosis of acidbase status. In the software, there are 13 different cases.

I addition to the software, You need the SA linear nomogram (to determine base excess (BE) for the 13 cases within the program). BE means the change of BB (sum of buffering bases in the blood).

To start the program in on the computers in datasalar Dot, Enter: login: Your personal student login lösen: Your personal student password Then wait a few seconds. Go to the startmenue, down to the left. Programs, SyraBas, SB SyraBas (click).

On the first page, read the information. Then click the mouse, and the program is running.

The program contains 13 cases. With the code number, You can see which of the 13 cases You are dealing with. The codenumber is found under ”help”. For example, if the code number is 45091, You are dealing with case 09 (compare the list of 13 cases).

Data about the patient can be obtained via five buttons:  the patientens leg  the bloodsample + bloodgas analyser  SA diagram on the wall  the urine sample  the timemachine to the right (gives information about how for example pH varied over time)

For each case , start by noting the code number. Then, find out about pH and pCO2 (data under blood sample) and BE (SA linear nomogram) HIT. Check

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additional dataif and when needed, test around! Characterize the acidbase status (acidosis/alkalosis, metabolic/respiratory sisturbance). Finally, go to the button ”state your conclusions”, and state the respiratory status, metabolic status, BE, - BB, and HCO3 for the patient. Consider the functional classification of the buffers of the blood (body fluids) how are the equilibria of the buffers become changed? Try to judge which of the 13 cases You are dealing with (compare the descriptions of the 13 cases). If possible, do all the 13 cases. Note down Your results, on the sheet in this compendium.

To finish, ”end program” and LogOff (startmenue).

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DESCRIPTION OF THE 13 CASES.

1. Young man with acute stop in airways (meatball stuck in throat) at time 0, relieved (cough up) after 1 minute. pH decrease when pCO2 goes up during 2 min, then normalised during 10 min. pO2 goes down to 9 during 2 min, normalised directly. Pulse increased to 145 directly, normalised during 10 min. Breathing frequency 0 initially, directly after relief 20/min, normalised during 10 min. Thus an acute respiratory acidosis, metabolic compensation never initiated.

2. Chronic, slowly progrediating emphysema. Gives a chronic respriratory acidosis. pCO2 up from 8 to 9 kPa during 4 weeks. Compensated by a secondary metabolic alkalosis.

- 3. Normal acid base status. Arterial blood: pH 7,4, pCO2 5,3 kPa, BE = 0, HCO3 = 24 mM, pO2 12,4 kPa, urine pH 5,8.

4. Patient and doctor at high altitude. Chronic oxygen deficit (pO2 low) results in hyperventilation. Gives a chronic respiratory alkalosis which is compensated by a secondary metabolic acidosis. Thus less acid is excreted in urine compared to the normal condition, and the urinary pH is increased. Consider 2,3-BPG.

5. Pronounced diabetic ketoacidosis, coming in for treatment. Unconscious since 3 h before admission to hospital. During 2 days before admission, pH and BE have gradually decreased. Bretahing has increased, resulting in lowered pCO2 (respiratory compensation). All normalised during one day and night, following admission.

6. Patient vomiting. During 2 days pH increases, BE becomes +15, pCO2 increased (compensation). Also renal mechanisms strive to lower the pH, thus urine pH has - increased (HCO3 secreted with urine).

7. Pregnancy, third trimester. Hyperventilation in late part of pregnancy is normal. Leads to a slight chronic respiratory alkalosis, with metabolic compensation, BEslightly negative.

8. Hyperaldosteronism (or liquorice overconsumption). Leads to hypokalemia and metabolic alkalosis (renal mechanism). OBS the not so common combination of increased pH in blood, and a low urinary pH. Respiratory compensation.

9. Decreased glomerular filtration rate (GFR). Bad excretion of protons (from non- volatile acid) in urine, leads to metabolic acidosis, BE has decreased continuosly. Respiratory compensation.

10. Headtrauma with hyperventilation. During 3 h pCO2 has been decreasing, down to 3,8 kPa. Leads to respiratory alkalosis. Almost no metabolic compensation, BE = -4 as the lowest value.

11. Infusion of 50 mmol HCl to healthy test person. During infusion pH has been gouing down, and BE down to -8. Respiratory compensation leads to a decreased pCO2. All normalised within one day and night.

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12. Patient in respirator, with a 10 min accidental hyperventilation. Leads to acute respiratory alkalosis. Breathing frequency constant 12. pCO2 down to 3,5 kPa, normalised quickly.

13. Coronary infarction leading to bad pump function, and arythmias complicate the situtaion further. Lack of oxygen in the entire organism leads to anaerobic metabolism with accumulation of lactate, a metabolic acidosis. During 10 min the pulse has been approx 95 and irregular. pO2 down to 9 kPa, BE down to -4. At time -1 minute, pulse 110, clearly irregular, BE further decreasing to -12. Arrythmias could be relieved (temporarily cured). During 20 min pO2 goes up to 12 kPa. During 15 h BE has become normalised. Consider 2,3-BPG.

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Syrabas-balans, results Name: Group: Datum:

Patient 1. Code number: pH pCO2 BB BE - HCO3