Lab 2 Acid base - Blood gas Flashcards
Isohydria
pH
The conc of H-ions in the body
Normal pH in blood
7.35-7.45
Isohydria is essential for two things in the body:
Any pH change can lead to:
Cell membranes
Enzyme activities
Electrolyte imbalance
Why is a buffer system needed in the body
Because hydrogen ions are constantly produced from chemical reactions, these can lead to alterations in pH
Definition of a buffer system
A solution that can maintain a nearly constant pH if diluted, or if small amounts of strong acids or bases are added: they resist pH changes
What does a buffer solution typically consist of?
Weak acid/base and one of its salts
If H+ in the body starts to increase, the conjugate base can uptake this excess.
If H+ starts to decrease, more weak acids can dissociate
What is the most important buffer system in all fluid compartments of the body?
Carbonic acid - bicarbonate system
Phosphate buffer, protein buffer
Three most important buffer systems of blood plasma
Carbonic acid - bicarbonate system
Primary - secondary phosphate buffer
Albumin - albumin + H+
Three most important buffer systems of RBCs
Carbonic acid - bicarbonate system
Primary - secondary phosphate buffer
Haemoglobin + O2 - haemoglobin - H+
Three most important buffer systems of tissue cells
Carbonic acid - bicarbonate system
Primary - secondary phosphate buffer
Cytoplasmic proteins
What does the vital buffer system consist of?
The kidneys and lungs
Buffering capacity of lungs
Can retain or excrete CO2 to regulate pH acutely
Reduced ECF pH - hypercapnia
Ventilation is stimulated (huge capacity)
Kussmaul breathing is observed (deep exp/ins)
Buffering capacity of kidneys
Can retain or excrete H+ and effectively regenerate the HCO3- via complex tubular mechanisms
Takes hours/days
Acid base sample
Sample: Ca-equilibrated Li-heparinised blood
Arterial: shows respiratory function
Air contamination must be avoided (false high pO2)
CO2 can evaporate into air: false low pCO2
Long storage: metabolism of RBCs: false high pCO2
Acid base method
ISE to measure pH and CO2
Based on the measured parameters, HCO3- and ABE can be calculated
Measured at 37 C
Solubility of gas is dependent on temp - has to be corrected according to temp of patient (hypo/hyper-thermia)
Give respiratory parameters
pCO2
Give metabolic parameters
HCO3- (depends on pCO2)
ABE
SBE
TCO2
Total CO2
5% higher than plasma HCO3-
Gives no direct information about respiratory function
SBE
Standard base excess
Same as ABE but calculated value
ABE
Actual base excess
the amount of acid/base needed to equilibrate blood to pH 7.4
Evaluation of Acid/Base state
- Evaluate acidosis/alkalosis according to pH!
Most important step - Search for cause of pH alteration
Respiratory/metabolic changes
Resp: pCO2 change Met: HCO3-, ABE change - Evaluate whether compensation effort is visible
Compensated state
Within 7.35-7.45
Below or above and it is decompensated
Respiratory background of pH alteration
pCO2 shows a strong shift in the same direction as pH
High pCO2 = bound to water = H2CO3 (carbonic acid)
= shift in acidic direction
Low pCO2: hyperventilation, too much CO2 is exhaled
Metabolic background of pH alteration
Lactic acid production: acidic shift of both parameters
ABE: positive in alkalosis, negative in acidosis
Evaluation of respiratory and metabolic parameters compared to pH
Evaluate whether the change of parameters correspond to the alteration of pH
How to detect compensatory effect?
The given parameter is shifted in the opposite direction compared to the pH
EXAMPLE:
Metabolic acidosis, the lungs will try and compensate by Kussmaul breathing. Result:
pH acidic
CO2 alkaline
Mixed acidosis
Advanced acidosis
All parameters are shifted significantly in the same direction as pH
Metabolic acidosis causes (8)
HCO3- loss Increased acid intake Increased acid production Grain overdose in cattle (VFA overproduction) Increased ketogenesis Decreased acid excretion Ion exchange (hyperkalaemia) Ethylene-glycol toxicosis
Metabolic acidosis effects (5)
Kussmaul breathing Hypercalcaemia: mobilization (long term) Vomiting, depression Hyperkalaemia Acidic urine
Metabolic acidosis treatment:
Adequate ventilation
if pH <7.2: alkaline (NaHCO3) infusion therapy (based on ABE calculation)
Anion gap
Cations:anions
Useful when attempting to determine cause of metabolic acidosis
Maintaining electroneutrality (anion gap)
Conc of cations and anions must be equal in plasma
Decrease in HCO3- has to be balanced by an increase in Cl- or Unmeasured anions
Direct HCO3- loss: Cl- replaces HCO3-
Normal anion gap: hyperchloraemic metabolic acidosis
If reduction of HCO3- is due to acc of Ua, Cl- stays normal
Increased anion gap: normochloraemic metabolic acidosis
Normal anion gap: hyperchloraemic metabolic acidosis
CAUSES
Diarrhea
Early kidney failure
Renal tubular acidosis
Acidifying substances
Increased anion gap: normochloraemic metabolic acidosis
CAUSES
Azotaemia/uraemia
Lactoacidosis
Ketoacidosis
Toxicosis
(basically substances in the blood that aren’t measured)
Metabolic alkalosis causes (5)
Increased alkaline intake (rotten/bicarbonate)
Increased ruminal alkaline prod (high prot, low carb)
Decreased hepatic ammonia catabolism (liver failure)
Increased acid loss: vomiting, GDV, abomasal displacement
Ion exchange: hypokalaemia (HCO3- retention)
Metabolic alkalosis effects (4)
Breathing depression Muscle weakness - hypokalaemia Hypocalcaemia (ø bind to albumin) Ammonia toxicosis Arrythmia
Metabolic alkalosis treatment
Treatment of underlying electrolyte imbalance
Respiratory acidosis causes (7)
Upper airway obstruction
Pleural cavity disease
Pulmonary disease
Depression of central control of respiration
Neuromuscular depression of respiratory muscles
Muscle weakness
Cardiopulmonary arrest
Respiratory acidosis effects (5)
Dyspnoea Cyanosis Suffocation Muscle weakness Tiredness
Respiratory acidosis treatment
Assisting ventilation
Treatment of cause (oedema of lungs)
Milk anxiolytic/sedating drugs to decrease fear/excitement caused by hypoxia
Respiratory alkalosis causes (5)
Hyperventilation: Excitation Forced ventilation (anaesthesia) Epileptic seizures Fever, hyperthermia Interstitial lung disease
Respiratory alkalosis effects
Hyperoxia, decreased pCO2:pO2 ratio
Increased elimination of HCO3- by kidneys
Respiratory alkalosis treatment
Anxiolytic drugs
Breathing into paper bag
Why do we analyse blood gas?
Assess effectiveness of gas exchange (esp during dyspnoea or anaesthesia
Blood gas analysis sample
Arterial blood (venous blood only gives indication of how much oxygen was consumed by body) Ca-equilibrated Li-heparinised plasma Closed sampling method (Avoid air contamination)
Blood gas analysis method
ISE
Standardized temp 37C (must be temp corrected!)
paO2
Arterial partial pressure of oxygen
Indicates the lungs ability to oxygenate blood
paCO2
Arterial partial pressure of carbon dioxide
Indicates the ability of alveolar gas exchange to remove CO2
SAT/SatO2
Oxygen saturation %
Indicates fraction of oxygen-saturated hemoglobin relative to total hemoglobin in the blood
Venous: 75-80%
Arterial: 90-100%
FiO2
Fraction of inspired oxygen
The assumed % of O2 concentration participating in gas exchange in the alveoli
Room air: 20.9%
>0.5 risk of O2 toxicity
What can be the case when paO2 is under 40-50 mmHg?
Cyanosis
Which is higher, pvCO2 or paCO2
pvCO2
Hypoventilation causes (5)
Upper airway obstruction
Pleural effusion
Disturbance to central control of respiration
Neuromuscular disease which affects resp system
Overcompensation of metabolic alkalosis
Hypoventilation effects
Dyspnoea, cyanosis
Hypoventilation treatment
Assisting ventilation
Diuretic treatment (fluid acc in lungs or thoracic cav)
Mild anxiolytic/sedative treatment
V/Q
Ventilation-perfusion mismatch
Hyperventilation causes
Iatrogen
Seizures
Excitation (mild/extreme)
Compensation of severe metabolic acidosis
