Acidosis? Flashcards

1
Q

A 68 year-old man with a history of very severe COPD (FEV1 ~ 1.0L, <25% predicted) and chronic carbon dioxide retention (Baseline PCO2 58) presents to the emergency room complaining of worsening dyspnea and an increase in the frequency and purulence of his sputum production over the past 2 days. His oxygen saturation is 78% on room air. Before he is place on supplemental oxygen, a room air arterial blood gas is drawn and reveals: pH 7.25, PCO2 68, PO2 48, HCO3- 31. What is the acid-base status of this patient?

A

The patient has a low pH (acidemia)

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2
Q

What is the diagnosis of the patient?

A

The patient has a high PCO2 (respiratory acidosis) and a high bicarbonate (metabolic alkalosis). The combination of the low pH and the high PCO2 tells us that the respiratory acidosis is the primary process.
The metabolic alkalosis is the compensatory process. The pH is still low despite this metabolic compensation.

Summary: Primary respiratory acidosis with compensatory metabolic alkalosis.

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3
Q

Define normal pH and define alkalosis and acidosis

A
  • normally pH is 7.4 and very tightly regulated within a normal range
  • if higher than 8 or lower than 6.8 it is incompatible with life
  • if pH is 7.35 or lower, this is termed acidosis (which depresses the CND, and leads to extreme conditions such as coma and respiratory failure)
  • if pH is 7.45 or higher, this is considered alkalosis (stimulates SNS, and leads to extreme conditions such as muscle seizures and convulsions)
  • Therefore, acidosis starts at an alkaline pH, but is acidic relative to the reference scale
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4
Q

Distinguish between metabolic and respiratory acid-base disorders

A

Respiratory
- A result of abnormal Pco2
- Lung disease, hypoventilation, hyperventilation
### Metabolic
- A result of something other than abnormal Pco2
- A high-protein diet, a high-fat diet, heavy exercise, excessive vomiting, severe diarrhea

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5
Q

How does the respiratory system function as a buffer?

A
  • acidic pH leads to dramatic increase in ventilation rate
    • alkaline pH leads to decrease in ventilation rate, though not as dramatic as acid, to maintain breathing ^[hypoventilation drive is less]
  • more ventilation leads to positive change: more CO2 out, acid elimination
  • less ventilation leads to negative change: lessCO2 out, acid retention
  • normal: no pH change
  • Respiratory system acts as a **physiologic buffer.
  • Acts rapidly and prevents severe [H+] changes (until kidneys help with remaining imbalance).
  • Buffering power **1-2 times that of all extracellular fluid chemical buffers combined.
    • demonstrates essential role in maintaining balance
  • If pH disturbance is outside the respiratory system, it can’t fully return pH to normal.
  • Effectiveness ranges from 50-75% ^[i.e. of change]
  • Example: pH falls from 7.4 to 7.0, respiratory system can return pH to ~7.2 - 7.3 (within 3 to 12 minutes).
  • Note: this process happens quickly
  • exercise not considered hyperventilation, though ventilation increases
  • generate more CO2, need to breathe more to reach isometabolic line
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6
Q

Is the respiratory system an effective buffer?

A
  • If pH disturbance is outside the respiratory system, it can’t fully return pH to normal.
  • Effectiveness ranges from 50-75% ^[i.e. of change]
  • Example: pH falls from 7.4 to 7.0, respiratory system can return pH to ~7.2 - 7.3 (within 3 to 12 minutes).
  • Note: this process happens quickly
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7
Q

Describe the extreme consequences of acidosis and alkalosis

A
  • acidosis (which depresses the CND, and leads to extreme conditions such as coma and respiratory failure)
  • alkalosis (stimulates SNS, and leads to extreme conditions such as muscle seizures and convulsions)
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8
Q

Discuss the role of bicarbonate in respiratory acid-base balance? Why is it so important?

A
  • Bicarbonate is a major buffer in the blood. Why is it so important?
    • Components are abundant: [HCO3-] = 24 mM, [CO2] = 1.2 mM (constant generation, despite low concentration).
    • System is open
    • regulated by both lungs and kidneys.
  • Bicarbonate **participates in reactions converting H+ to CO2 and vice versa.
    • when H is high, it bind bicarbonates ions
    • if CO2 concentration increases, more H and HCO3 are formed
  • Acidosis occurs if CO2 levels build up.

Note that the pK is 6.1.
This is not close to the optimal pH.
But bicarbonate buffer operates in an open system.
Other mechanisms work in tandem with buffering to maintain 20:1 ratio and thus optimal pH.
Mechanisms include actions of lung: breathing and hyperventilating, kidney: synthesising HCO3 and excreting H+.

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9
Q

Describe the significance of the Aa gradient

A

The alveolar-arterial oxygen difference is 17 mmHg. This value is elevated, suggesting that the hypoxemia is due to either shunt or areas of low V/Q (the more likely explanation in a patient with COPD) and cannot be explained by hypoventilation alone.

A-a Gradient: in general, >20mmHg suggests pathological shunt ^[n.b. can’t clinically measure, A-a gives proxy]

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10
Q

Define shunts and describe their clinical relevance

A
    • Shunt: Blood bypasses ventilated lung areas a.k.a does not undergo gas exchange, e.g. passing unventilated alveoli ^[in other words: venous blood enters arterial circulation]
    • Venous Admixture: amount Mixed venous blood added to end-capillary blood to produce observed difference between arterial and pulmonary-end capillary blood
  • shunted blood by definition is not exposed to ventilated alveoli
    • Increased concentration O2 in alveoli, therefore, won’t improve O2 in shunted blood
      • may slightly increase SaO2 if only a small shunt ^[e.g. oxygenating post-op anaesthetic patient, lung bases collapsed, poorly ventilated–worsens with age, size]
    • > 30% shunt : unlikely to see SaO2 changes ^[need to solve structural issue]
  • A-a Gradient: in general, >20mmHg suggests pathological shunt ^[n.b. can’t clinically measure, A-a gives proxy]
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11
Q

List some anatomical and pathological causes of shunt

A
  • Anatomical (e.g. thesbian ^[drain heart] and bronchian veins ^[drain lung])
    • Pathological: anything that impairs gas getting to, and across, the alveolar membrane (pneumonia, atelectasis…)
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12
Q

Define obstructive lung diseases and describe how they present in lung function tests

A

Obstructive Disorders (Airflow Limiting)
- Obstructive respiratory disorders reduce airflow due to airway narrowing i.e. an inability to blow out quickly
- Reduced maximum expired flows due to:
- airway lumen narrowing e.g. bronchitis and mucus
- airway wall thickening and inflammation: causing reactive airways e.g. asthma
- loss of lung elastic recoil e.g. in emphysema ^[can take up to 20s to fully exhale] and COPD

Note also: overlap syndrome (Asthma and COPD) ^[ACOS]

Coving in OLD

  • increased resistance to airflow, increased RV and TLC (air trapped)
  • decreased FVC and FEV1
  • decreased FEV1/FVC ratio
  • decreased MEF
  • left shift of curve, indicating higher TLC, and slower downward slope (coving?)
    • note PIF also decreased, though not a s dramatic as PEF

Air trapping defined as disproportionate increase in residual volume (RV) or RV/TLC ratio.
- RV/TLC ratio of > 120%: Mild air trapping
- RV/TLC ratio of > 140%: Moderate
- RV/TLC ratio of > 160%: Severe

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13
Q

List and describe some indications for LFT

A
  • Diagnosing and assessing patients with respiratory symptoms (cough, wheeze, phlegm, dyspnoea)
  • Assessing smokers, those exposed to pollution, and those with family history of respiratory disease
  • Differentiating between respiratory and cardiac causes of breathlessness ^[exam questions]
  • Screening high-risk populations for respiratory disease
  • Evaluating treatment response
  • **Pre-operative risk assessment for anesthesia and abdominal/thoracic surgery (e.g. pulmonary exercise tests)
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14
Q

List some causes of mixed acid-base disorders

A
  • Low pH
  • Low [HCO3-]
  • High Pco2 ^[i.e. increase/decreases out of sync - shorthand to see if there is compensation or not]
    Examples include:
  • Respiratory and metabolic acidosis due to chronic pulmonary disease and acute episode of diarrhea
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15
Q

What is the role of the kidney in acid base balance?

A

Kidneys excrete and reabsorb H and HCO2
- kidneys are responsible for 25% compenstation of acids not handled by lungs
- they do this via direct and indirect mechanisms
- directly: excreting or reabsorbing hydrogen ions
- indirectly: excreting or reabsorbing bicarbonate buffer

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16
Q

Describe the actions of the kidney in acidosis and alkalosis

A

In acidosis the kidneys do two things:
- secrete hydrogen ions by primary and secondary active transport mechanisms. Examples include:
- buffering protons with ammonia and phosphate
- making new bicarbonate ions from carbon dioxide and water
- synthesise ammonia (HCO3 is a by-product of this process)

In alkalosis:
- processes are reversed: excrete the bicarbonate and reabsorb hydrogen ions (to help bring down the alkaline pH)

17
Q

Describe how the kidney would compensate for acidosis

A

all HCO3 is essentially reabsorbed
modulated by hydrogen ion/ proton secretion
additionally, it is regulated by H concentration gradient: more H, more efficient

	   -  proton concentration in tubule is key
h2co3 formed
ca on tubular side, results in co2 formed
h2co3 reformed in cell
ca leads to regeneration of hco3
na/hco3 and cl/hco3 export HCO3 into blood
Note: Na/K/ATPase contributes to exchanger function
	
	
	
	
activity and expression of key H and HCO3 transporters is also regulated and affects efficiency e.g. by acidity levels
    in acidosis (secretion is favourable, therefore) increased H- ATPase in collecting duct, and Na/H antiporter and Na/3HCO3 expression and activity is increased in proximal tubule
18
Q

Does secretion of bicarbonate typically occur? Under what conditions?

A

Secretion of HCO3 in collecting duct
NOTE: ONLY in alkalosis
- co2 diffuses into cell
- hco3 exchanged for cl
- h pumped with ATPase into interstitial space and blood, helping to correct

19
Q

Before the intervention of the lung, what measures would the body take to correct pH?

A
  • Chemical buffers are the first line of defense against changes in blood pH.
  • Largest buffer pool in the body is in extracellular fluid (HCO3-/CO2, Inorganic H2PO4-, Plasma Proteins).
  • Intracellular fluid contains cellular proteins (e.g., Hb), organic HPO4-, HCO3-/CO2.
  • Bone serves as a buffer with mineral H2PO4- and mineral HCO3-.
  • Chemical buffers minimize pH changes **but don’t remove acid or base from the body.
  • Buffering power varies: ECF rapid (minutes), ICF/bone (hours).

How good a buffer depends on:
- its abundance
- mineral H2po4 found in large stores in bone
- its pKa (i.e. if close to optimal pH)
- H2PO4 = 6.8, close, not the best
- HPPO4 = pK ~ pHi

N.B. proteins largest buffer pool in body, in both ECF and ICF