Chapter 048. Acidosis and Alkalosis (Part 12)

Chia sẻ: Thuoc Thuoc | Ngày: | Loại File: PDF | Số trang:8

Thêm vào BST

Báo xấu

87
lượt xem 4
download

Download Vui lòng tải xuống để xem tài liệu đầy đủ

Metabolic Alkalosis Associated with ECFV Expansion, Hypertension, and HyperaIncreased aldosterone levels may be the result of autonomous primary adrenal overproduction or of secondary aldosterone release due to renal overproduction of renin. Mineralocorticoid excess increases net acid excretion and may result in metabolic alkalosis, which may be worsened by associated K + deficiency. ECFV expansion from salt retention causes hypertension. The kaliuresis persists because of mineralocorticoid excess and distal Na + absorption causing enhanced K+ excretion, continued K+ depletion with polydipsia, inability to concentrate the urine, and polyuria. Liddle's syndrome (Chap. 278) results from increased activity of the collecting duct Na+...

Chủ đề:

Bình luận(0) Đăng nhập để gửi bình luận!

Lưu

Nội dung Text: Chapter 048. Acidosis and Alkalosis (Part 12)

Chapter 048. Acidosis and Alkalosis (Part 12) Metabolic Alkalosis Associated with ECFV Expansion, Hypertension, and Hyperaldosteronism Increased aldosterone levels may be the result of autonomous primary adrenal overproduction or of secondary aldosterone release due to renal overproduction of renin. Mineralocorticoid excess increases net acid excretion and may result in metabolic alkalosis, which may be worsened by associated K + deficiency. ECFV expansion from salt retention causes hypertension. The kaliuresis persists because of mineralocorticoid excess and distal Na + absorption causing enhanced K+ excretion, continued K+ depletion with polydipsia, inability to concentrate the urine, and polyuria.
Liddle's syndrome (Chap. 278) results from increased activity of the collecting duct Na+ channel (ENaC) and is a rare inherited disorder associated with hypertension due to volume expansion manifested as hypokalemic alkalosis and normal aldosterone levels. Symptoms With metabolic alkalosis, changes in central and peripheral nervous system function are similar to those of hypocalcemia (Chap. 346); symptoms include mental confusion, obtundation, and a predisposition to seizures, paresthesia, muscular cramping, tetany, aggravation of arrhythmias, and hypoxemia in chronic obstructive pulmonary disease. Related electrolyte abnormalities include hypokalemia and hypophosphatemia.[newpage] Metabolic Alkalosis: Treatment This is primarily directed at correcting the underlying stimulus for HCO 3– generation. If primary aldosteronism, renal artery stenosis, or Cushing's syndrome is present, correction of the underlying cause will reverse the alkalosis. [H +] loss by the stomach or kidneys can be mitigated by the use of proton pump inhibitors or the discontinuation of diuretics. The second aspect of treatment is to remove the factors that sustain the inappropriate increase in HCO 3– reabsorption, such as ECFV contraction or K+ deficiency. Although K+ deficits should be repaired, NaCl
therapy is usually sufficient to reverse the alkalosis if ECFV contraction is present, as indicated by a low urine [Cl–]. If associated conditions preclude infusion of saline, renal HCO 3– loss can be accelerated by administration of acetazolamide, a carbonic anhydrase inhibitor, which is usually effective in patients with adequate renal function but can worsen K+ losses. Dilute hydrochloric acid (0.1 N HCl) is also effective but can cause hemolysis, and must be delivered centrally and slowly. Hemodialysis against a dialysate low in [HCO3–] and high in [Cl–] can be effective when renal function is impaired. Respiratory Acidosis Respiratory acidosis can be due to severe pulmonary disease, respiratory muscle fatigue, or abnormalities in ventilatory control and is recognized by an increase in PaCO2 and decrease in pH (Table 48-7). In acute respiratory acidosis, there is an immediate compensatory elevation (due to cellular buffering mechanisms) in HCO3–, which increases 1 mmol/L for every 10-mmHg increase in PaCO2. In chronic respiratory acidosis (>24 h), renal adaptation increases the [HCO3–] by 4 mmol/L for every 10-mmHg increase in PaCO2. The serum HCO3– usually does not increase above 38 mmol/L. Table 48-7 Respiratory Acid-Base Disorders
I. Alkalosis II. Acidosis A. Central A. Central nervous system stimulation 1. Drugs 1. Pain (anesthetics, morphine, 2. sedatives) Anxiety, psychosis 2. Stroke 3. Fever 3. 4. Infection Cerebrovascula r accident B. Airway 5. Meningitis, 1. encephalitis Obstruction 6. 2.
Tumor Asthma 7. Trauma C. Parenchyma 1. B. Hypoxemia Emphysema or tissue hypoxia 2. 1. High Pneumoconiosi altitude, PaCO2 s 2. 3. Pneumonia, Bronchitis pulmonary 4. Adult edema respiratory 3. distress Aspiration syndrome 4. 5. Severe anemia Barotrauma
C. Drugs or D. hormones Neuromuscular 1. 1. Pregnancy, Poliomyelitis progesterone 2. 2. Kyphoscoliosi Salicylates s 3. 3. Cardiac failure Myasthenia 4. D. Stimulation Muscular of chest receptors dystrophies 1. E. Miscellaneous Hemothorax 2. Flail 1. chest Obesity
3. 2. Cardiac failure Hypoventilatio n 4. Pulmonary 3. embolism Permissive hypercapnia E. Miscellaneous 1. Septicemia 2. Hepatic failure 3. Mechanical hyperventilatio n 4. Heat exposure
5. Recovery from metabolic acidosis