PHYS: Acid/Base Balance Flashcards
(28 cards)
1
Q
normal blood pH
A
- 7.35-7.45
2
Q
volatile vs non-volatile sources of acidity
- example
- where do they come from?
- how are they removed?
A
- volatile (can become gaseous): carbonic acid - comes from CO2, removed via respiratory system
- non-volatile: sulfuric, lactic, uric and ketoacids - comes from metabolism, removed renally
3
Q
bicarbonate buffer
A
- CO2 combines with H2O to form carbonic acid, which dissociates into H+ and HCO3-
- open buffer system: resp system can change breathing rate and renal system can make more bicarbonate
- think equilibrium shifts
4
Q
protein buffer
A
- amino acids contain ionisable groups (COO- or NH3+)
- most important = histidine
- largest buffer system
5
Q
CO2 transport in blood
A
- CO2 diffuses out of somatic cells, across endothelium and into capillaries
- in RBC: combines w/ H2O to form carbonic acid (most CO2), which dissociates into HCO3- and H+
- Hb picks up some CO2 and H+, HCO3- mops up excess H+
6
Q
phosphate buffer
A
- can get phosphate from inorganic phosphate (Pi), ADP/ATP, phospholipids, bones
- allows kidneys to excrete H+ ions while generating new bicarbonate
7
Q
how is bicarb recycled in the kidney
A
- bicarb and H+ from filtrate join to make carbonic acid, which breaks down into water + CO2
- CO2 enters the PCT cell and combines with H2O to form new carbonic acid, which breaks down into H+ and bicarb
- H+ pumped back out of the cell and into filtrate via antiporter to join with another bicarb > cycle repeats
- bicarb goes back into systemic circulation
8
Q
where is bicarb reabsorbed?
A
- 80% in PCT
- 10% in thick ascending limb of LoH
- 10% in DCT/CD
9
Q
how does the kidney generate new bicarb to combat acidosis?
A
- glutamine > glutamate > bicarb
- this also forms ammonium (weak acid) which goes back into filtrate, combines with Cl- to become neutralised and gets excreted
10
Q
medullary recycling
A
- ammonium competes with K+ for the NKCC2 transporter
- ammonia in filtrate goes back out into interstitium
- creates concentration gradient, causing NH3 to move back into CD and mop up H+ > forms NH4+ to eliminate acid
11
Q
how is pH fine tuned
A
- 2 types of cells in collecting duct
- during Acidosis, A-intercalated cells secrete H+ via either H+ ATPase pump of H+/K+ antiporter and reabsorbs HCO3-
- during alkalosis, B-intercalated cells (betas fight basic bitches) secrete HCO3- into filtrate for excretion and reabsorbs H+
12
Q
factors affecting bicarb reabsorption
A
- ang II enhances Na+/H+ pump in PCT for Na+ reabsorption = pushing more H+ out into filtrate
- aldosterone enhances H+/K+ ATPase pump in a-intercalated cells in CD = secretes more H+ into filtrate
- acidosis = more bicarb reabsorbed
- hyperkalaemia: K+ competes with NH4+ for NKCC2 transporter = less bicarb reabsorbed
- decreased GFR = more time for bicarb reabsorption
13
Q
metabolic vs respiratory disturbances
A
- metabolic: reduced (acidosis) or elevated (alkalosis) bicarbonate
- respiratory: reduced (alkalosis) or elevated (acidosis) pCO2
14
Q
acidosis vs acidaemia
A
- acidosis = the process that decreases arterial blood pressure
- acidaemia = arterial blood pH <7.35
15
Q
normal pCO2 and normal HCO3-
A
- pCO2 = 35-45 mmHg
- HCO3- = 22-26 mmol/L
16
Q
3 lines of mechanisms to maintain acid-base balance
A
- buffer system (bicarbonate, phosphate, protein)
- respiratory: chemoreceptors detect H+ levels and modify breathing
- renal: reabsorption of HCO3- and secretion of H+ ions
17
Q
how is minute volume related to pCO2?
A
- inversely proportional i.e. decreased minute volume (ventilation) = increased pCO2
18
Q
acute vs chronic respiratory acidosis
A
- acute: sudden elevation of pCO2 (>45 mmHg) due to failed ventilation e.g. drugs, obstruction, asthma etc
- chronic: long-term decreased reflexive response to hypoxia and hypercapnia e.g. restrictive lung disease with V/Q mismatch, COPD
19
Q
examples of metabolic acidosis
A
- diabetic ketoacidosis, lactic acidosis, severe diarrhoea (loss of HCO3-)
20
Q
what is the anion gap?
- how is it calculated?
- what is a normal anion gap?
A
- difference between cations and anions to assess electrolyte balance and diagnose metabolic acidosis
- anion gap = Na - (Cl + HCO3)
- 9-14 mmol/L (if higher = metabolic acidosis)
21
Q
toxins that can cause metabolic acidosis
A
- MULEPAK
- Methanol (+ other alcohol)
- Uraemia due to renal failure
- Lactic acid
- Ethylene glycol
- Paraldehyde + other drugs
- Aspirin toxicity/OD
- Ketones (starvation, alcoholic and diabetic ketoacidosis)
22
Q
what is hyperchloraemic acidosis + causes
A
- type of metabolic acidosis (decreased HCO3-) with normal anion gap (9-14 mmol/L) but elevated chloride
- ingestion of chloride acids, failure to excrete HCl, infusion of chloride-rich fluids e.g. saline
23
Q
causes of respiratory alkalosis
A
- hyperventilation (increased removal of CO2)
- anxiety
- medications
24
Q
how to classify acute vs chronic respiratory alkalosis
A
- depends on degree of metabolic compensation
25
causes of metabolic alkalosis
- vomiting (loss of H+)
- diuretics
- excessive intake of alkaline drugs e.g. antacids
- hypovolaemia = buildup of bicarbonate
- inadequate renal excretion of HCO3-
26
general Sx of acid-base imbalance (acidosis OR alkalosis)
- seizures
- lethargy and confusion
- light-headedness
- N&V
- tachycardia
27
which compensatory mechanism will fix which type of acid/base imbalance?
- respiratory system will compensate for metabolic acidosis/alkalosis
- renal system will compensate for respiratory acidosis/alkalosis
28
Boston bedside rules
- 6 rules to assess degree of compensatory response to acid/base imbalance, once the initial imbalance has been diagnosed clinically via ABG + Hx
- if compensation has not occurred, can indicate a second acid/base disorder (mixed disturbance)
