PBL 8 Flashcards
Tachycardia
increased heart rate greater than 100bpm, this is greater than what is normal
Tachypnoea
increase respiratory rate increased from what is normal
Ringer’s Lactate
– solution for fluid and electrolyte replacement. Isotonic with blood. Lactate has alkaline effect which can help counteract the acidosis (it is metabolised into HCO3-).
Anion gap
difference between primary measured
cations (Na+ and K+) and primary measured anions
(Cl- and HCO3-) in blood serum or in urine.
Creatine
waste molecule generated from
metabolism of creatine in muscle. Filtered by
kidneys and disposed in urine.
What kind of acidosis did she have
hyperchloraemic metabolic acidosis
describe her results and what they mean pH HCO3 pCO2 Anion gap
pH - acidosis
HCO3- = 5 (very low)
-> metabolic acidosis – fits with history of diarrhoea and high creatinine in bloods
pCO2 = 16 (low)
-> respiratory compensation (hyperventilation to blow off excess CO2)
Anion gap = 10 (normal) with high chloride -> hyperchloraemic metabolic acidosis
Causes of high versus normal anion gap
Normal anion gap (hyperchloraemic metabolic acidosis):
Severe diarrhoea (loss of HCO3-)
Reduced kidney H+ excretion
(HCO3- decreased, Cl- increased to compensate)
High anion gap: Lots of causes but main ones: Ketoacidosis Lactic acidosis (HCO3- decreased, unmeasured anions increase so high anion gap).
How do you compensate for acid base distrubances
Physiological buffers (super fast)
- Bicarbonate-carbonic acid buffering system
- Protein buffers (intracellular and extracellular)
- Phosphate buffers in the bone
Pulmonary compensation (slower) – ventilation
Renal compensation (really slow, starts 6h after sustained acidosis/alkalosis)
Describe haemoglobin buffer system/bicarbonate
In tissues: CO2 + H2O H2CO3 H+ + HCO3- H+ + Hb HHb In lungs: HHb releases H+ (and takes up O2) Then ....H+ + HCO3- H2CO3 H2O + CO2
describe and explain her blood results
- Low potassium
- High Cl-
- high creatinine
- K+ low – in acidosis, high H+ in blood (acidaemia). H+ moves into cells (buffers) so K+ moves out of cells to maintain electroneutrality. But in this case, K+ lost due to diarrhoea.
- High Cl- - compensatory increase in Cl- due to loss of HCO3-.
- High creatinine – decreased renal function
Explain the blood pressure
Also note BP changes indicating postural hypotension due to dehydration. Postural hypotension = abnormal fall in BP at least 20mmHg systolic and/or fall of 10mmHg diastolic within 3 min of standing upright
How do you replace fluid
Usually use crystalloids – saline, Lactated Ringers etc
Remain longer in ECF
Isotonic
describe the fluid balance homeostasis
Fluid volume decreases
-> increased Na+ concentration in blood
-> increased osmolarity
-> detected by hypothalamus (an osmoreceptor)
-> stimulates posterior pituitary to secrete ADH (anti-diuretic hormone)
-> feel thirsty so drink
kidneys retain water -> reduced volume of concentrated urine
water conserved in ECF
what are the symptoms of metabolic acidosis
- headache
- decreased blood pressure e
- muscle twitching
- warm flushed skin
- nausea, vomitting, diarrhoea
what are the causes of metabolic acidosis
DKA severe diarrhoea - causes loss of bicarbonate renal failure shock - diabetic ketoacidosis
what was her metabolic acidosis complicated by
dehydration
describe respiratory compensation
- A drop in pH, results in increased ventilation to blow off excess CO2.
- An increase in pH decreases ventilatory effort, which increases PCO2 and lowers pH back towards normal.
describe renal compensation
In acidosis, kidneys excrete H+ in urine and retain HCO3-.
• In alkalosis, kidneys excrete HCO3- and retain H+ in the form of organic acids.
what also acts as a buffer
• Lastly, bone may also serve as a buffer because it contains a large reservoir of bicarbonate and phosphate and can buffer a significant acute acid load. Patients who have low albumin levels and bone density due to malnutrition or chronic disease, and anaemic patients, have an ineffective buffering capability.
describe potassium in metabolic acidosis
- In presence of an H+ load, H+ ions move from the extracellular fluid into the intracellular fluid. For this to occur, potassium moves outside the cell into the extracellular fluid to maintain electroneutrality
• So I.V. potassium is given to patients early in treatment, despite the often-elevated serum potassium level
what is the compensation in the kidney that is used to treat metabolic acidosis
Acute • Blood buffers • Nonvolatile buffers absorb excess H+ • Compensation • Respiratory • • rate increased, eliminates CO2 Renal • Secrete H+ and reabsorb and generate HCO3-
what is respiratory alkalaemia caused the next day
• In this case the central chemoreceptors
are slow at responding to the reversal in bicarbonate and so the compensatory hyperventilation is still functional
• Bicarbonate will slowly enter the brain interstitial fluid over about a 12 to 24 hour period and the central chemoreceptor inhibition will be progressively eliminated.
• The recovery of pCO2 to normal lags behind the rise in the bicarbonate.
how do you do simple dehydration check
- dehydration urine colour chart
describe the effect of water loss on performance
- 1% loss of body mass = dehydration
- 2% = impaired performance
- 4% capacity for muscular work reduced
- 6% heat exhaustion
- 8% hallucination
- 10% circulatory collapse and heat stroke