Acid- Base Balance

Systems for acid-base regulation

1) Buffer system
- fast acting system, primary regulator of acid-base balance
- major buffer system of ECF is carbonic acid(H2CO3) bicarbonate (HCO3), others include, phosphate, protein, & Hb
(p.1278)
- the cell acts as buffer by shifting of H+ in and out of the cell
- when ECF lvl of H+ ↑(Acidosis), H+ enters the cells for exchange of K+, which may result in hyperkalemia
- when ECF lvl of H+↓ (Alkalosis), H+ enters the plasma from the cells in exchange for K+ hypokalemia

2) Respiratory System ( CO2=↑H+, ↑acidity of the blood, ↓pH)

 when CO2 enters RBC & combines with H2O to form H2CO3. H2CO3 dissociates H+ + HCO3-. The free H+ is
buffer by the Hb molecules & the HCO3- diffuse  plasma
 this process revers at the pulmonary capillaries
 the amount of CO2 in the blood directly relates to H2CO3 & H+ []
 w/ ↑ respiration, less CO2 remains in the blood less H2CO3 and less H+ molecuels
 w/ ↓respiration, more CO2 remains in the blood more H2CO3 levl and more H+ molecules
 ( the medulla & brainstem has the respiratory center to control rate of CO2 excretion ， if CO2 or H+ ↑, the
 respiratory centers stimulate ↑ RR & depth for breathing ( hyperventilation)
 RR are inhibited if the center sense low H+ or CO2 lvl ( Hypoventilation)

3) Renal system
- kidneys can generate addition HCO3 & eliminate excess H+ as compensation for acidosis
- respiratory imablances affect carbonic acid [], metabolic imbalances affect the base bicarbonate
- acidosis can caused by an ↑ in carbonic acid (respiratory acidosis), or decrease in bicarbonate ( metabolic acidosis)
- alkalosis can be caused by ↓ in CA ( respiratory alkalosis) or an increase in HCO3- ( metabolic alkalosis)

Respiratory acidosis (Carbonic acid excess)

- occurs w/ hypoventilation, results in buildup of CO2 lvl in blood, causing ↑{H+}, ↓pH
COMPENSATION: kidney conserves HCO3- & secrete H+ in urine
- serum HCO3 is usually normal in acute situation, kidneys start to compensate in 24 hr

Respiratory alkalosis
- CA deficit, occurs with hyperventilation
- primary cause: hypoxemia from pulmonary disorder ( pneumonia, pulmonary embolism),
- hyperventilation can occur as a physiological response to metabolic acidosis and increase emtabloic demands ( ex/. A
state of fever), . pain, anxiety and other CNS disorder can cause an increase in respirations, w/ physiological needs
- the ↓ in the arterial CO2 levels lead to a ↓ in [CA] in blood and increase in pH
COMPENSATION; a ↓ HCO3 lvl differentiates compensated respiratory alkalosis from acute OR uncompensated
respiratory alkalosis

Metabolic acidosis ( base bicarbonate deficit)

- occurs when an acid other than CA accumulates int eh body or when HCO3- I slost form body fluid
bicarbonate deficits
 Ex/. Ketoacid accumulation in DKA and lactic acid accumulation in shock
- severe diarrhea results in loss of bicarbonate
- in renal disease, the kidnesy lost their abilities to reabsorb bicarbonate & secrete H+
 COMPENSATION: ↑ CO2 excretion by the lunngs, developing Kussmal’s respiration (deep, rapid breathing), the
kidney attempts to excrete additional acid
 If metabolic acidosis is present, calculating the anion gaps helps determien the SOURCE of acidosis.
 ANION GAP: the difference b/w the measured serum cations and anions in the ECF, normal anion gap is 8-
16mmol/L, ↑in metabolic acidosis ass/ w/ acid gain ( lactic acidosis), but normal in metabolic acidosis is caused by
bicarbonate loss (diarrhea)

Metabolic alkalosis (Base bicarbonate excess) occurs when acid is lost as a result of promote vomiting or gastric
sucntion or when HCO3- ↑ ( from ingestion of baking soda)
COMPENSASTION: ↓respiratory rate to ↑ plasma CO2. However, oncres hypoxemia occurs or plasma CO2 reaches a
certain lvl, stimulation of the chemoreceptors ↑ RR. Renal excreation of HCO3- occurs
Week 3 Respiratory system
Pneumonia
 an acute inflammation of the lung parenchyma, caused by microbial agents
 protective mechanism of the airway, filtration of air, warming and humidification of inspired air,
epiglottis closure over the trachea, cough reflex, mucocillariy escalator mechanism, secretion fo IgA,
alveolar macrophase

Factors predisposing to pneumonia

 decreased consciousness depresses the cough and epiglottal reflexes, allow aspiration of oropharygnheal contents
 lungs
 tracheal intubation interfere normal cough reflex & mucociliary escalator mechanism
 the ciliary escalator mechanism is ipared by air pollution, cifgarette smoking, viral URIs, gaining
 malnutrition alters lymphocytes and polymophonuclear leukocytes
  disease such as leukemia, ETOH, DM are asso. w/ increased risk of Gram negative bacilli (abnormal flora in the
respiratory tract)
 altered oropharyngeal flora can also occur secondary to Ab therapy given of an infection somewhere else in the
body

Acquisition of Organisms
1) Aspiration from the nasopharyc or oropharynx
2) Inhalation
3) Hematogenous spread form primary infection site
ypes of pneumonia

Community-Acquired pneumonia Hospital-acquired Aspirati on Penumonia Opportunisti c pneumonia

(CAP) pneumonia

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resulti ng pneumonia.
Risk - smoking, immunosuppressive therapy, H x o f l o s s c o n s c i o u s n e s s ( r e s u- l t s e v e r e p r o t e i n c a l o
factors - presence of COPD, general debility, o f s e i z u r e s , a n a e malnutriti s t h e son, i a , h e a d
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Types of -S. pneumoniae Pseudomonas, Enterbacter, S u b s t a n c e s o t h e r t h a n b a c t e r i a
organism - a t y p i c a l o r g a n i s m ( e x / . L e g i o n e lSl aaureus,
, MRSA. may be aspirated into the lung,
Mycoplasma, Chlamydia, viral S. pneumoniae s u c h a s g a s t r i c c o n
exogenous chemical contents, or
irritati ng gases.