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Lecture notes on pathophysiology-acid-base balance disorder II
(1) concept:

The decrease of pH caused by the primary decrease of plasma [HCO3-].

(ii) Reasons

Main reasons:

Too much fixed acid, HCO3- loss =

1. bicarbonate-too much loss

(1) Too many direct losses:

(2) Blood dilution reduced HCO3- concentration.

2. Excessive loss of fixed acid and HCO3 buffer:

(1) overproduction of fixed acid:

① Lactic acidosis.

(2) ketoacidosis:

(2) Excessive intake of exogenous fixed acid:

① Salicylic acid poisoning

② Excessive intake of chlorine-containing acid-forming drugs.

(3) Immobilized acid excretion disorder

3. Hyperkalemia:

Potassium ion and intracellular hydrogen ion exchange

H+ secretion in epithelial cells of distal convoluted tubule decreased.

(Abnormal alkaline urine)

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(3) Classification

1.AG adds acid substitution.

Features: AG is elevated and blood chlorine is normal.

Mechanism: plasma fixed acid ↑.

2. normal acid replacement of 2.AG

Features: AG is normal and blood chlorine is elevated.

Mechanism: HCO3- loss =

(D) compensatory adjustment of the body

Each regulation mechanism has played a role in succession.

1. Buffering effect of extracellular fluid

2. Compensatory regulation of lung

3. The buffering effect of cells

4. Compensatory regulation of kidney

(5) Blood gas characteristics

PH antimony carbon dioxide AB BB BE

(vi) Effects on the body

1 cardiovascular system

(1) arrhythmia

(caused by hyperkalemia)

(2) Decreased myocardial contractility

(Competing with calcium to bind troponin; Inhibit calcium influx; Inhibiting the release of calcium from sarcoplasmic reticulum)

(3) The reactivity of vascular system to catecholamine is decreased.

Central nervous system: central inhibition

Mechanism:

GABA production increased; ATP production decline

3 electrolyte metabolism: hyperkalemia

Mechanism:

The exchange of hydrogen and potassium inside and outside the cell increased; The kidneys excrete more hydrogen and less potassium.

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(7) Prevention and control principles

Prevention and treatment of primary disease with 1

2. Improve microcirculation and maintain electrolyte balance.

3 Application of alkaline drugs

Two. respiratory acidosis

(1) concept:

The decrease of pH caused by the primary increase of PaCO2 _ 2 (or H _ 2O _ 3).

(ii) Reasons

The main causes: pulmonary ventilation disorder and excessive inhalation of CO.

1. Pulmonary ventilation disorder

Respiratory center depression, respiratory muscle paralysis, airway obstruction, chest and lung diseases; Improper use of ventilator

2. excessive 2. Carbon dioxide inhalation

(2) Classification

1. Acute respiratory acidosis

2. Chronic respiratory acidosis

(D) compensatory adjustment of the body

1. Intracellular ion exchange and intracellular buffering (main compensation for acute respiratory acid)

(1) intracellular hydrogen ion-potassium ion exchange

(HCO 3-Cl- exchange inside and outside RBC.

Results: Blood pH increased, blood potassium increased and blood chlorine decreased.

2 Compensatory regulation of kidney (mainly to compensate chronic respiratory acid)

(5) Blood gas characteristics

(6) Impact on the body: Basically, acid generation is more serious than acid generation.

(7) Prevention and control principles

1 acid

2. Strengthen the management of ventilator.

Three. metabolic alkalosis

(Metabolic alkalosis)

(1) concept:

The increase of pH caused by the primary increase of plasma [HCO3-].

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(ii) Reasons

Main reasons:

H+ loss, HCO3- overload

1.H+ is missing.

(1) stomach lost

Lose H+

Chlorine loss (low chlor-alkali poisoning)

Loss of potassium ion (hypokalemic alkalosis)

Body fluid loss

(2) Renal damage

(the influence of drugs, the influence of diseases)

2. Bicarbonate overload

3. Transfer of H+to cells

Hypokalemia:

Potassium ion and intracellular hydrogen ion exchange

H+ secretion of epithelial cells of distal convoluted tubule increased.

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(abnormal aciduria)

(3) Classification

1. Salt reactive alkalosis

Features: Due to insufficient effective circulating blood volume or low chlorine content.

2. Salt-tolerant alkalosis

Features: aldosteronism or hypokalemia.

(D) compensatory adjustment of the body

Each regulation mechanism has played a role in succession.

1. Buffering effect of extracellular fluid

2. Compensatory regulation of lung

3. Intracellular and extracellular ion exchange

4. Compensatory regulation of kidney

(5) Blood gas characteristics

PH antimony carbon dioxide AB BB BE

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(vi) Effects on the body

1 central nervous system: central excitation

Mechanism: (1)GABA decreased.

(2) The oxygen dissociation curve shifts to the left → hypoxia in brain tissue.

2. neuromuscular: excitability-(decrease of blood free calcium)

3. Hypokalemia

(7) Prevention and control principles

Prevention and treatment of primary disease with 1

2 Correct blood pH value

Patients with salt-reactive alkalosis were given isotonic or semi-isotonic saline.