MindMap Gallery Pathophysiology – Acid-base disorders
Pathophysiology-acid-base balance disorders, including regulation of acid-base balance, Indicators of acid-base balance disorders, etc. It is recommended to study by yourself with the textbook!
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This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
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Acid-base balance disorder
Note
↑
increase/expand/activate/promote
↓
reduce/shrink/suppress
-
No change/little change
Source of acid and alkali
acid
Volatile acid-H2CO3-pulmonary discharge
Fixed acid->metabolite-renal excretion
base
>Food
Regulation of acid-base balance
blood buffer
>Bicarbonate buffer system
Features
Strong buffering capacity, quick response, not durable
Adjustable openness
The lungs regulate CO2; the kidneys regulate HCO3-
Buffers fixed acids, does not buffer volatile acids
Phosphate buffer system
>Intracellular/tubular
protein buffer system
Plasma Protein-Buffer H
Hemoglobin-bound CO2-buffered volatile acids
Histiocyte Buffering
Ion exchange (H-K exchange, Cl-HCO3 exchange)
Acidosis-blood K↑
Alkalosis-Blood Cl↑
Phosphate buffer system
Pulmonary acid discharge
PaCO2↑-central chemoreceptor-breathing↑-H2CO3↓
H↑, PaCO2↑, >PaO2↓-peripheral chemoreceptor-breathing↑-H2CO3↓
Kidneys excrete acid and maintain alkali
proximal tubule
Reabsorption of NaHCO3
Blood H↑-carbonic anhydrase activity↑-HCO3 reabsorption↑
Secrete H, NH4
PH dependence-acidosis↑-secretion of NH4↑
Distal convoluted tubule, collecting duct
Reabsorption of NaHCO3
Cl-HCO3 exchange
Alkalosis-kidney reabsorption of HCO3↓-blood Cl↑
Supplement Cl chlorine (HCO3)
secrete H
H-Na exchange and K-Na exchange inhibit each other
Acidosis-blood K↑
Indicators of acid-base balance disorders
PH
7.35-7.45 (7.4)
HCO3/H2CO3=20
PaCO2
33-46(40)mmHg
Reflects respiratory acid-base balance disorder
SB and AB
Standard Bicarbonate SB - HCO3 under standard conditions - reflects metabolism
Actual bicarbonate AB - HCO3 after isolation from air - reflects respiration and metabolism
Normal AB=SB, 22-27 (24)
Buffer base BB
45-52 (48) mmol/L
>HCO3-reflects metabolism
Base remaining BE
The amount of acid ( )/base (-) required to titrate whole blood to pH=7.4 under standard conditions - (-3- 3)
reflect metabolism
Anion gap AG
AG=Undetermined anion UA—Undetermined cation UC=Na-(HCO3 Cl)=10-14 (12)
Na, HCO3, Cl-can measure cations/anions; anions-acid ions are not measured
AG>16-AG increased acid substitute
type
Acid substitute
concept
Fixed acid↑, HCO3 loss↑-plasma HCO3↓
blood gas analysis
Original-SB, AB, BB↓, BE negative value↑
Secondary-PaCO2↓, AB<SB
Classification
AG enhanced acid substitute
AG↑, blood Cl-
Fixed acids other than HCl↑
Fixed acidosis, severe renal failure
AG normal type acid substitute
AG-, blood Cl↑
HCO3↓with compensatory Cl↑
Diarrhea, mild to moderate renal failure, renal tubular acidosis, carbonic anhydrase inhibitors, hyperkalemia
HCO3重吸收↓/泌H↓
body compensation
>Lungs
H↑-Peripheral chemoreceptors-Respiration↑-PaCO2↓, AB<SB
blood, tissue cells
Buffer-SB, AB, BB↓, BE negative value ↑, blood K↑
kidney
Acid excretion and alkali preservation (H, NH4, HCO3)-acidic urine
H-Na exchange↑, Na-K exchange↓-row K↓
H↑-carbonic anhydrase activity↑-HCO3 reabsorption↑
Influence
cardiovascular
Myocardial contractility↓
H↑
Ca-troponin binding↓
Ca influx↓
Sarcoplasmic reticulum Ca release↓
troponin
Vascular Catecholamine Sensitivity↓-↑Vascular-Blood Pressure↓
H↑
ventricular arrhythmias
Blood K↑
central depression
H↑
Biological oxidase activity↓-ATP↓
Glutamic acid decarboxylase activity↑-GABA↑ (inhibitory neurotransmitter)
skeleton
Rickets, osteomalacia
H↑-bone calcium release
substitute alkali
concept
Base↑, H loss↑-plasma HCO3↑
blood gas analysis
Original - SB, AB, BB↑, BE is positive ↑
Secondary-PaCO2↑, AB>SB
Body compensation - the opposite of acid metabolism
Influence
Heart
Arrhythmia
Hypokalemia
central excitement
PH↑
Glutamic acid decarboxylase activity↓-GABA↓
Hemoglobin O2 affinity ↑ - oxygen dissociation curve shifts to the left - O2 release ↓ - cerebral hypoxia
neuromuscular hyperactivity
PH↑-free Ca↓-muscle excitability↓
Acid breath
concept
CO2 emitted↓/inhaled↑-plasma H2CO3↑
blood gas analysis
Original-PaCO2↑、AB>SB
Secondary - SB, AB, BB↑, BE positive ↑ (respiratory acidity with compensated alkali)
body compensation
Acute acid breathing
>Tissue Cell Buffering
Ion exchange
intracellular buffer
Hemoglobin buffer
Chronic acid breathing
kidney
Expelling acid and maintaining alkali
Influence
homoacid
Central symptoms are more obvious
CO2↑Direct↑Vascular-Intracranial Pressure↑
CO2 anesthesia - confusion, tremors, delirium, drowsiness
Respiratory alkali
concept
Hyperventilation-Plasma H2CO3↓
blood gas analysis
Primary-PaCO2↓, AB<SB
Secondary - SB, AB, BB↓, negative BE value ↑ (respiratory alkali with compensatory acidity)
body compensation
Acute respiratory alkali
Histiocyte Buffering
Ion exchange
intracellular buffer
Chronic respiratory alkali
kidney
Influence
congeneric base
More prone to dizziness, abnormal sensation in limbs and around mouth
CO2↓directly↓blood vessels