Abb ions

Buffer mechanisms

 Blood
Bicarbonate CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3–
Hemoglobin
 Lungs
 Kidneys
 Osmolarity
2Na + urea+ glucose
Why is it imp?
 Base excess
BE = BB - normal BB
Normal values: 0±2 mmol/l
It is defined as the amount of strong acid that would need to be added to the test sample to bring
the pH to 7.4, assuming that ABR respiratory failure is excluded (ie, pCO 2 = 5.3 kPa). In
metabolic acidosis, it would be necessary to add a strong base; the corresponding parameter is
referred to as the lack of bases , base deficit , BD, or (more often) is expressed as negative BE.
 Osmolar gap
The osmolar gap is the difference between the measured osmolality and the calculated osmolarity.
The difference in units is attributed to the difference in the way that blood solutes are measured in
the laboratory versus the way they are calculated.
Clinically the osmolar gap is used to detect the presence of an osmotically active particle that is
not normally found in plasma, usually a toxic alcohol such as ethanol, methanol or isopropyl
alcohol
Normal parameters of abg

7.35-7.45
Metabolic Acidosis
Anion gap = [Na + K] - [HCO3 + Cl]
How do we know if compensation is
adequate ?
B) respiratory acidosis
•Airway obstruction;
•neuromuscular causes (stem damage, depression of the respiratory center, myasthenia,
botulism , tetanus , ...);
•reduction of the breathing area - pneumothorax , hemothorax, pneumonia , ...;
•circulation disorders – embolism ;
•poorly performed artificial respiration .

•Chronic respiratory acidosis -hypercapnia initially stimulates the respiratory center,

with pCO 2 above 9 kPa – depression – the stimulation at that moment is mainly
hypoxemia → do not give pure oxygen!!!
•COPD ;
•chronic sedative overdose ;
•primary alveolar hypoventilation ;
•Pickwick syndrome ;
•neuromuscular disability;
•anatomical deformity of the chest - kyphoscoliosis , ...;
•terminal stages of pulmonary fibrosis .
 c) Respiratory alkalosis
• Anxiety or panic
• Fever
• Overbreathing (hyperventilation)
• Pregnancy (this is normal)
• Pain
• Tumor
• Trauma
• Severe anemia
• Liver disease
• Central nervous system (brain) abnormalities
• Overdose of certain medicines, such as salicylates, progesterone
D) Metabolic alkalosis

 Vomiting
 Contraction alkalosis- Decreased extracellular volume triggers the
renin-angiotensin-aldosterone system, and aldosterone subsequently stimulates
reabsorption of sodium (and thus water) within the nephron of the kidney. However, a
second action of aldosterone is to stimulate renal excretion of hydrogen ions (while
retaining bicarbonate), and it is this loss of hydrogen ions that raises the pH of the blood.
 Esp due to loop and thiazide diuretics
 Cystic fibrosis
 Alkalotic agents
 shift of hydrogen ions into intracellular space – Seen in hypokalemia. Due to a low
extracellular potassium concentration, potassium shifts out of the cells. In order to maintain
electrical neutrality, hydrogen shifts into the cells, raising blood pH.
 Hyperaldosteronism
 Kalemia 3.5-5mEq/L
where is k= higher? In cell or extracellularly
Hypokalemia hyperkalemia
Intake Decreased ->Fasting , Increased-> iv fluid

Cellular shift Insulin intake , alkalosis, refeeding Crush injury , tumor lysis
syndrome syndrome ,acidosis,hyperosmolarity,

excretion Increased ->Vomiting , diarrhea, Decreased-> aki,conns syndrome ,

diuretic use , hyperaldosteronism ACE I ,k+sparing diuretics
 Case 1
26 year old man was shot in the abdomen. He arrested in the ambulance and
resuscitaion was commenced. Sinus rhythm with normal QRScomplexes was
restored. Aggressive volume loading in the Emergency Department resulted in a
systolic pressure of 70 mmHg just prior to transfer to theatre for immediate
laparotomy. External cardiac massage and volume loading were continued
as pulseless electrical activity due to hypovolaemia continued. Adequate circulation
was restored following surgical control of bleeding and volume loading with colloid.
Hyperventilation with 100% was continued and initial blood gases were collected
20 minutes later.
When the initial gas results were received, management was to increase the minute
ventilation to lower the pCO2 further and to continue volume resuscitation with
colloid, crystalloid and red cell concentrate to achieve an endpoint of systolic BP
greater then 110 systolic. Urine output was good. Bicarbonate was not given.
Postoperatively, the patient was transferred ventilated to the Intensive Care Unit.
Total intraoperative fluids was about 20 litres including 16 units of packed red cells

What do you think the acid base disorder is ? What do you think the etiology is ?
 Abdominal trauma (due gunshot wound) resulting in hypovolaemic cardiac
arrest & lactic acidosis (due to poor perfusion).
Case 2
 This middle-aged obese man was admitted following a motor vehicle crash. Previous
health was good.
 Examination: His major injury was chest trauma with a small right pneumothorax and
at least five fractured ribs on the right. There was no head or neck injury. Abdomen
was soft. He was haemodynamically stable with BP 130/80 and pulse 90/min. Heart
sounds were normal. Respiratory distress was present. Respiratory rate was 30/min.
Saturation was 95% on high flow oxygen via face mask.
 pH 7.18
 pCO2 73 mmHg
 pO2 93 mmHg
 HCO3 27 mmol/l

This man has an acute respiratory acidosis due to acute chest trauma. This patient has
respiratory failure and requires intubaton and ventilation.
 Case 3
 „An 8-year-old boy presents to the emergency department with a 2- hour history of vomiting
after eating dinner at a seafood buffet.
 Arterial blood gas analysis reveals a pH of 7.50, an bicarbonate level of 34 mEq/L, and partial
carbon dioxide pressure of 40 mm Hg. Which of the following best describes the acid-base
disturbance occurring in this patient?
 (A) Metabolic acidosis
 (B) Metabolic acidosis/respiratory acidosis
 (C) Metabolic acidosis/respiratory alkalosis
 (D) Metabolic acidosis/respiratory compensation
 (E) Metabolic alkalosis
 (F) Metabolic alkalosis/respiratory compensation“1
 Vomiting typically induces a metabolic alkalosis due to a loss of hydrogen ions from the
stomach, leading to an increase in pH. This leaves an increased bicarbonate concentration
(generally >24 mEq/L) in the bloodstream. In this case, the partial carbon dioxide pressure is
still normal; thus, no respiratory compensation has occurred, and the patient has
uncompensated metabolic alkalosis.
Case 4

 A 19-year-old woman with a severe gastrointestinal infection presents to the emergency department with a 5-day history of
vomiting and diarrhea.
 Serum chemistry tests show: Na+: 138 mEq/L K+: 3.0 mEq/L Cl–: 88 mEq/L HCO3–: 21 mEq/L BUN: 10 mg/dL Creatinine: 0.8
mg/dL Glucose: 101 mg/dL Arterial blood gas analyses shows a pH of 7.38, partial arterial carbon dioxide pressure of 37 mm
Hg, partial arterial oxygen pressure of 82 mm Hg, and an oxygen saturation of 96% on room air. Which of the following
statements is most accurate regarding this patient’s acid-base status?
 (A) She has a metabolic acidosis
 (B) She has a mixed metabolic alkalosis and metabolic acidosis
 (C) She has a mixed respiratory alkalosis and respiratory acidosis
 (D) She has no acid-base disturbances
 (E) She has a respiratory alkalosis
 While this patient’s pH, bicarbonate, and carbon dioxide levels are all very close to normal, it is always important to look
more closely before concluding that there is no disorder. Vomiting is a common cause of a metabolic alkalosis, while diarrhea
is a common cause of non-anion-gap metabolic acidosis. The patient has had gastrointestinal symptoms that have led to
acute dehydration, which indicates that these symptoms are probably quite severe. It is also important to look at the serum
chemistry. One would expect a hypokalemic hypochloremic metabolic alkalosis from vomiting, but only the electrolyte
deficiencies are present.
 The equalized pH suggests that the patient is losing an equal amount of acid through vomiting as she is base through
diarrhea. Therefore, it is more likely that she has a mixed acid-base disorder than no electrolyte imbalances at all
Case 5

 5 yo male, admitted for suicide attempt. Has ingested large amount of aspirin. At
admission somnolent, difficult to make contact with
 Br 30 min
 hr 100 min
 BP 142/88, t = 36.8 °C
 Toxic levels of salicylates,
 pH 7.25
 pCO2 14 mmHg
 HCO3 - 8 mmol/l
 what is the dx ?
Case 6
36 year old female presents to the emergency department with complaints of nausea over
the past few days and one day of non-bloody, non-bilious emesis. The patient was recently
pregnant and delivered a baby girl a few months ago. Although she has been having
difficulty keeping food and fluids down, she is continuing to breast feed her daughter. The
patient denies any diarrhea, illicit drug use, or toxic ingestions. Physical exam is notable
for dry mucous membranes and tachycardia. The patient is otherwise afebrile, with a blood
pressure of 120/80 mmHg, heart rate of 126 beats per minute, respiratory rate of 16 breaths
per minute, and an oxygen saturation of 100% on room air.
Ddx ?
Now what do u think it is ?

 The patient was transferred to the ICU for further management of her severe metabolic acidosis. The
following day, her condition improved. Serum/plasma toxicology labs were negative for propylene glycol,
ethylene glycol, salicylate, or acetaminophen. The initial immunoassay urine drug screen was negative and no
illicit substances were found on urine comprehensive drug screen by gas chromatography/mass spectrometry.
 A volatile alcohol panel by gas chromatography-headspace showed no detectable amounts of ethanol,
isopropanol, or methanol, but was positive for acetone at 30 mg/dL. Beta-hydroxybutyrate levels were
elevated at 6.88 mmol/L (RR: <0.28 mmol/L).
 Repeat lactic acid remained elevated at 2.1 mmol/L. Follow up arterial blood gas labs showed an
improvement in the patient's elevated anion gap metabolic acidosis (Table 3).. Random urine organic acid
testing by gas chromatography/mass spectrometry showed a severe lactic aciduria with ketonuria. Blood and
urine cultures were negative and antibiotics were discontinued. The patient noted that she was feeling better
and was able to eat food. Her physical exam had also improved. She was transferred out of the ICU and later
discharged in stable condition
 Ans Elevated anion gap metabolic acidosis due to starvation ketoacidosis, in the
setting of lactation.
Case 7

 8 yo female, DM 1st type Chills and fever lasting several days She has not felt well => not eaten much and not
taken much insulin During admission day: Abdominal cramps,
vomited several times Physical exam: Br 30 min
,HF 112 min
BP 110/70 lying and 100/60 standing, 37 °C,
Dry mucosae and fruity breath odor
pH 7,20
pO2 96 mm Hg
pCO2 21 mm Hg
HCO3- 8 mmol/l
Glc 15 mmol/l
Na+ 148 mmol/l
K+ 5,5 mmol/l
Cl 110 mmol/l
Positive acetone in urine

 What is the diagnosis?

Case 8

 A 68-year-old woman is brought to the emergency department because of shortness of

breath and a 4.5 kg (10 lbs.) weight gain over the past two weeks. Her pulse is 105 per
minute and blood pressure is 160/84 mm Hg. Physical examination of the neck reveals
bilateral jugular venous distension. The abdomen is soft and nontender but a positive
fluid wave is present. The extremities show 2+ bilateral pitting edema. She is admitted
to the medicine service for treatment. Intravenous furosemide is administered and
diuresis of 5 L of fluid occurs in a relatively short time. The following data were
collected from the patient before and after receiving furosemide.
 which of the following is the most likely explanation for the acid-base abnormality in this patient?
 A. Decreased plasma aldosterone.
 B. Hyperkalemia.
 C. Hyperventilation.
 D. Hypoventilation.
 E. Loss of extracellular fluid.

 The patient is showing the signs and symptoms of "contraction alkalosis," a type of metabolic alkalosis
caused by diuretic-induced loss of extracellular fluid.
 Loop diuretics (such as furosemide) and thiazides can cause rapid and significant urinary fluid excretion, as
seen in our patient. This decreases extracellular fluid (ECF) volume and hence relieves symptoms associated
with edema, but it concentrates ECF HCO3-, causing a metabolic alkalosis. In our patient's case, furosemide
treatment has decreased ECF volume by 5L, causing [HCO3-] to rise from 24 mEq/L to 35 mEq/L, and
serum pH to rise to 7.49.
Case 9

 A 46-year-old man is found unconscious on the bathroom floor by his family. The
family states the patient has a medical history significant only for depression and
gastroesophageal reflux disease (GERD). His medications include escitalopram and
omeprazole.
 Upon arrival to the emergency department the patient is more responsive but still
confused and drowsy. A few episodes of vomiting are noted. On exam, the patient is
afebrile with a blood pressure (BP) of 90/50 mm Hg, respiratory rate (RR) of 24 breaths
per minute, and heart rate (HR) of 120 beats per minute (bpm). His pupils are reactive
to light with a nonfocal neurologic exam
 He has dry mucous membranes and mild diffuse abdominal tenderness to palpation. No
alcoholic fetor is noted.
 Laboratory studies are as follows: Na 132 mEq/L, K 3.4 mEq/L, Cl 90 mEq/L, serum
bicarbonate (HCO3) 10 mEq/L, BUN 60 mg/dL, Cr 1.6 mg/dL, and glucose 80 mg/dL.
Arterial blood gas (ABG) reveals a pH of 7.2 and PCO 2 of 25 mm Hg. Serum ethanol,
acetone, and serum β-hydroxybutyrate are negative. The measured serum lactate is 1.6
mmol/L. Urinalysis reveals 4+ calcium oxalate crystals.
 Dx ethylene glycol poisoning
Case 10
Ans : respiratory acidosis with some
metabolic compensation .
 A 17-year-old patient admitted to the hospital with congestive heart disease and
scoliosis . Upon admission, the laboratory was examined and again 24 hours later.

admission