ACIDOSIS - production of H+
■ TISSUE METABOLISM- 12 500meqldCO2
* LIVER utilization of AMA lor gluconic gene sis
Hi504, HjPOa 3 major H* load......        50 nraqMay
- STRENUOUS EXERCISE........lactic acid
■ DIABETES MELLITUS ...... ketoacidosis
. INGESTION OF ACIDS, DIARRHOEA
. FAUILURE OF KIDNEY
ALKALOSIS
•Vomit
•Fruits, vegetables
Consequence of pH disturbances
• Change of tertiary and quaternary structure of proteins
• I of activity of enzymes
• changes in permeability of membranes ■   changes in distribution of electrolytes
Regulation of pH of body fluids
■ Buffer systems... immediately, small capacity
■ Lungs,., co, ...quickly, limited capacity • Kidney...h\hco3 .slowly, high capacity
BUFFERS - BUFFER CAPACITY OF BLOOD
* BUFFER-weak acid
+ The Hendeison-Hasselbalch equation
HA       H* + A-
<= + H*    JiJdMl stiffly iod
Relative acidity of weak acids is expressed by t--.--.--r constant ■ Negative logarithm of d .const, is pK ...it is pH.st which
concentration of W and UDdissociated molecules equals
pH=pK + log [A-]/[AH] Trie highest buffering capacity if pH =pK buffer capacity of Wood ■ 48rnmol/l
BUFFERS IN BLOOD
- Plasma proteins dissociate
Free carboxyl: R-COOH R-COO-+ H* Free aminogroups: R-NHj' <=>R-NHS* H*
• Hemoglobin (histidin residua)
Buffering capacity 6« I lhanthat of proteins Hb is weaker acid than HbO.=>
Hb is better buffer than HbCV'l buffering capacity in lungs-egsier release of CO, . opposite effect in tissue helps binding CO, 1
■ Phosphates   H?POj «:=> HPO,*+.H*
• Bicarbonate system HCO/ + H+
K-(|lia.lion 27- 15
co, + H,0 J=« HtC.O,        H- + uco,
co, + M,(I^»H- + iico3 Unnonr, w* can Jeliue a dissociation wtisLnni for int<
„ _ ih-JIIUCO,) ~ JCOJ
In VigWWhiiiir torn, this equal Urn becomes:
Equation 77-17
k:o,i
Finally. » tMprWB lCO,\ In icrnib of Pc.03. "Tailing,
iium Henry's Law ihm |coj — s ■ l'£_L3,:
Equation ■.!:■!
pH = pK + lag
[HCOjl
DISTURBANCES OF ACID/BASE BALANCE
Physiologic value malab&lic
raspiialory
HCOy 20   hcd,1 HC03- HC03- HC03
CO,
1 CO, CO;
CO,
Compensation  h(p«rlli(paVMitllatiori Wdrceye-c.&alion
HCp,   HCO3"   HCO3" HCCy
>: CO;
CO-
COMPENSATION OF ACIDOSIS
NEAD OF NaHC03mmolfl: BE*0,3*WEIGHT
• Isotonic solution 1,39 % (0,167molfl)
"A of amount needed, new measurement, (examination of K+)
ACfDOBASIC BALANCE AND
MOVEMENT OF K* BETWEEN ECF AND ICF
PLASMATIC CONCENTRATIONS!-S.J mmolfl ECF
1 -t- »!■■-'    ' hypokallumi*
		«-	H*	
icr				
haliuiia
Dependence of kaliemie on pH - at a constant total content of K+
PH	7.2	7.4	7.6	
K+	4.9	4.0	3.2	mmol'J
	6.2	5.0	3.8	
	7.3	6.0	4.5	
Physiologic PLASMATIC CONCENT RAT I Oh 3.5 - E.3 mmo"!
METABOLIC ACIDOSIS
. CAUSES
T Production of acids (diabetes, loss of weight
anaerobic glycolysis) Loss of bicarbonate (diarrhea, inhibitors of
carbonic artftydrase} Intake ol acids
RenaE failure of add secretion
■ RESPIRATORY COMPENSATION
H* is bound IH* + HCOa- - H,0 + CO.) EXSPIRATION (Kussmaul respiration) ALKALIC RESERVE DECREASES
METABOLIC ALKALOSIS
- CAUSES
Loss of H* (vomit, deficiency of K*) Intake of bases
Production of bases (oxidation of lactate)
- RESPIRATORY COMPENSATION is limited - hyp oven tUation -hypoxia + CO, - sons -ol respiration
- EXCRETION of BICARBONATE by KIDNEY * TpH-ICa*,-*tetany
RESPIRATORY ACIDOSIS
• CAUSES
IVentilation (barbiturates) Reduction of lung's tissue
■ H* SUFFERED BY TJONBICARBQNATE BUFFERS
• EXCRETION of H* by KIDNEY lag by 1-2 days
RESPIRATORY ALKALOSIS
- CAUSES
hyperventilation (hypoxia, psychiatric)
- H* RELEASED BY NONBICARBONATE BUFFERS
• EXCRETION of BIKARBONATE by KIDNEY
- First aid - quieting, rebrealhing