Acid Base (Resp) Flashcards
What is normal pH range of arterial blood? [1]
What is normal pH range of venous blood? [1]
What is typical arterial blood pH? [1]
What is typical venous blood pH? [1]
What is normal pH range of arterial blood? [1]
7.35-7.45
What is normal pH range of venous blood? [1]
7.31-7.41
What is typical arterial blood pH? [1]
7.40
What is typical venous blood pH? [1]
7.35
Which organ controls CO2 levels? [1]
Which organ controls HCO3- levels? [1]
Lungs
Kidneys
Hessel bank equation xxx
What investigation would you conduct to find pCO2 and HCO3- values? [1]
ABG
What is the physiology behind the following?
1) Respiratory acidosis
2) Respiratory alkalosis
3) Metabolic acidosis
4) Metabolic alkalosis
1) Respiratory acidosis: inadequate pulmonary excretion of CO2 causes elevation blood pCO2
2) Respiratory alkalosis: excess pulmonary excretion of CO2 causes decrease blood pCO2
3) Metabolic acidosis: excess loss of bicarbonate via kidney or digestive tract or excess production of acid (H+) that consumes bicarbonate
4) Metabolic alkalosis: excess loss of protons via kidney or digestive tract
What are the two leading causes of respiratory acidosis? [2]
Name 3 others causes [3]
Hypoventilation and ventilation-perfusion mismatch resulting in inadequate excretion of CO2
Drugs suppress breathing (powerful pain medicines, such as narcotics, and “downers,” such as benzodiazepines), especially when combined with alcohol
Brain injury impairing CNS respiratory centres
Diseases of gas exchange (such as asthma and chronic obstructive lung disease)
Diseases of the chest (such as scoliosis), which make the lungs less efficient at filling and emptying
Diseases affecting the nerves and muscles that drive lung ventilation
Severe obesity, which restricts how much lungs can expand
Why does elevated pCO2 from ineffective resp excretion cause acidosis?
CO2 rises (without HCO3- compensation), causes right shift of:
CO2 + H20 ->/<- H+ + HCO3
but it takes days to occur / 3-5 days to maximise
Signs and Symptoms of Resp. Acidosis?
Symptoms:
- Headache
- Lethargy
- Anxiety
- sleepiness
- fatigue
- memory loss
- restlessness
- muscle weakness
Signs:
- drowsiness
- gait disturbance
- decreased deep tendon reflexes
- disorientation
- tremors
- myoclonic jerks
- papilloedema
- tachycardia
- cardiac dysrhythmias
- decreased blood pressure
- skin flushing (CO2 causes vasodilation).
Why does pH changes faster in CSF c.f. blood? [1]
Blood has proteins than can act as buffers, CSF does not
What is a CNS symptoms of resp. acidosis? [1]
Increased CO2 causes cerebral arterial vasodilation increased intracranial pressure with oedema – net result is a dreceased brain blood flow
If patient has acute CO2 retention, then signs and symptoms will be severe / subtle?
If patient develops chronic CO2 retention, signs and symptoms will be severe / subtle?
Explain xx
If patient has acute CO2 retention, then signs and symptoms will be severe
If patient develops chronic CO2 retention, signs and symptoms will be subtle
Because in chronic CO2 retention, kidneys and brains have time to compenste
Key ABG findings:
*If ACUTE respiratory acidosis blood pH will be low (acidaemia) and pCO2 in the blood will be high, usually over 6.3 kPa with normal plasma bicarbonate levels (no compensation).
If CHRONIC respiratory acidosis blood pH will be low normal (i.e. 7.35-7.40) or low (but not as low as expected for pCO2), pCO2 will be high and bicarbonate will be elevated*.
How do you treat respiratory acidosis? [4]
Treat cause !:
- Bronchodilator drugs to reverse some types of airway obstruction
- Noninvasive positive-pressure ventilation (sometimes called CPAP or BiPAP) or mechanical ventilation if needed
- Opioid drug overdose reversal with naloxone
- Oxygen if the blood oxygen level is low – BUT must be careful with oxygen
Why do you need to monitor when giving O2 to Ptx with respiratory acidosis? Especially if have COPD
- Giving oxygen to these patients may lead to worsening CO2 retention from ventilation-perfusion mismatch: causes more acidosis.
- Can lead to CO2 narcosis and cardio-pulmonary arrest
How should you treat hypoxaemia in Ptx with COPD and chronic hypercapnia? [2]
- Controlled oxygen therapy with **24% or 28% O2 **
- with target haemoglobin saturation of 88 – 92% as hypoxaemia is life threatening.
- If CO2 does go up and pH falls may need to mechanically ventilate patient.
How does metabolic compensation to respiratory acidosis occur? [3]
- Increase HCO3- reabsorbtion at PCT
- Produce and excrete more ammonia
- Produce and excrete more phosphate ions
Explain the mechanism of HCO3- reabsorption and how it reduces pH
Increasing renal HCO3- production will cause the equation to shift to left, decreasing H+ & raising pH
CO2 + H2O ⇌ HCO3- + H+
MoA:
- Protons pumped into tubules react with bicarbonate filtered from the blood (through glomerulus) to form CO2, via action of CA in inner tubule wall.
- CO2 then diffuses back into tubule cell & converted to bicarbonate via CA inside tubular cell. This process removes the filtered bicarbonate from the tubular fluid.
- When all luminal (inside tubes) bicarbonate has been converted to CO2 and reabsorbed, free protons continue to be pumped into urine.
- Bicarbonate and sodium in tubular cells are reabsorbed into capillary blood by a symport mechanism in basal tubular cell wall.
Explain how ammonia is excreted to reduce pH [1]
Explain how excretion of phopshate ions occurs to reduce pH [2]
Ammonia: combines with free protons to form ammonium ions. These ions carry protons into urine without raising the concentration of urine free protons.
Phosophate ions: combine the proton with monohydrogen phosphate anion. Adding proton forms dihydrogen phosphate anion which can be excreted in urine
What disease does excessive excretion of phosphate ions lead to? [1]
This requires phosphate which comes from breakdown of calcium phosphate in bone, which can lead to bone weakening and osteoporosis.
If someone is in acute respiratory acidosis they will have [] paCO2 (eg >6.3 kPa) and [] [HCO3-]. This means the ratio of [HCO3-]/pCO2 [] and thus pH [].
If someone is in acute respiratory acidosis they will have high paCO2 (eg >6.3 kPa) and normal [HCO3-]. This means the ratio of [HCO3-]/pCO2 decreases and thus pH also decreases
If someone is in chronic respiratory acidosis they will have [] paCO2 (eg >6.3 kPa) and [] [HCO3-]. This means the ratio of [HCO3-]/pCO2 is [] and thus pH is []
If someone is in chronic respiratory acidosis they will have high paCO2 (eg >6.3 kPa) and elevated [HCO3-] This means the ratio of [HCO3-]/pCO2 is restored and thus pH is normalized within the acidotic part of normal of 7.35-7.40 (FULL compensation) OR is close to normalisedbut still not normal (PARTIAL compensation).
When does respiratory alkalosis occur? [1]
Respiratory alkalosis generally occurs when person hyperventilates. Increased breathing produces increased alveolar respiration, expelling CO2 from circulation
Signs and symptoms of resp. alkolosis
Resp. alkalosis causes decreased Ca ions. (Many signs relate)
Symptoms:
acute cases hyperventilation is accompanied by dizziness, light headedness, confusion, agitation, and possibly blurred vision, cramps and tingling or numbing around the mouth and in the fingers and hands.
Signs
* Hyperventilation !
* Tachyopnea
* hyperpnea (deeper breaths than normal)
* muscle twitching
* hyperactive reflexes, spasms
* weakness
* seizures
* syncope
* irregular heart beats,
* tetany
*
Effect of resp. alkolosis / acidosis on free Ca2+ ions? [1]
Increase in pH (alkaemia), promotes increased calcium protein binding, which decreases free calcium.
Acidaemia decreases protein binding, resulting in increased free calcium.
How does resp. alkalosis cause syncope? [1]
What happens to O2 dissociation curve in resp alk?
1) Decrease CO2 content: of blood causes constriction of cerebral blood vessels – may cause syncope
2) Alkalaemia shifts the haemoglobin O2 dissociation curve to the left:, impairing O2 delivery to tissues.
3) pH related changes in free Ca2+ blood levels can lead to an increase in neuromuscular excitability- increased risk arrythmias and tetany (involuntary and sustained muscle contractions)
