Chapter 020. Hypothermia and Frostbite (Part 2)

Chia sẻ: Thuoc Thuoc | Ngày: | Loại File: PDF | Số trang:6

Thêm vào BST

Báo xấu

66
lượt xem 5
download

Download Vui lòng tải xuống để xem tài liệu đầy đủ

Thermoregulation Heat loss occurs through five mechanisms: radiation (55–65% of heat loss), conduction (10–15% of heat loss, but much greater in cold water), convection (increased in the wind), respiration, and evaporation (which are affected by the ambient temperature and the relative humidity). The preoptic anterior hypothalamus normally orchestrates thermoregulation (Chap. 17). The immediate defense of thermoneutrality is via the autonomic nervous system, whereas delayed control is mediated by the endocrine system. Autonomic nervous system responses include the release of norepinephrine, increased muscle tone, and shivering, leading to thermogenesis and an increase in the basal metabolic rate. Cutaneous cold thermoreception causes direct...

Chủ đề:

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

Lưu

Nội dung Text: Chapter 020. Hypothermia and Frostbite (Part 2)

Chapter 020. Hypothermia and Frostbite (Part 2) Thermoregulation Heat loss occurs through five mechanisms: radiation (55–65% of heat loss), conduction (10–15% of heat loss, but much greater in cold water), convection (increased in the wind), respiration, and evaporation (which are affected by the ambient temperature and the relative humidity). The preoptic anterior hypothalamus normally orchestrates thermoregulation (Chap. 17). The immediate defense of thermoneutrality is via the autonomic nervous system, whereas delayed control is mediated by the endocrine system. Autonomic nervous system responses include the release of norepinephrine, increased muscle tone, and shivering, leading to thermogenesis and an increase in the basal metabolic rate. Cutaneous cold thermoreception causes direct reflex vasoconstriction to conserve heat. Prolonged exposure to cold also stimulates the thyroid axis, leading to an increased metabolic rate.
Clinical Presentation In most cases of hypothermia, the history of exposure to environmental factors, such as prolonged exposure to the outdoors without adequate clothing, makes the diagnosis straightforward. In urban settings, however, the presentation is often more subtle and other disease processes, toxin exposures, or psychiatric diagnoses should be considered. After initial stimulation by hypothermia, there is progressive depression of all organ systems. The timing of the appearance of these clinical manifestations varies widely (Table 20-2). Without knowing the core temperature, it can be difficult to interpret other vital signs. For example, a tachycardia disproportionate to the core temperature suggests secondary hypothermia resulting from hypoglycemia, hypovolemia, or a toxin overdose. Because carbon dioxide production declines progressively, the respiratory rate should be low; persistent hyperventilation suggests a central nervous system (CNS) lesion or one of the organic acidoses. A markedly depressed level of consciousness in a patient with mild hypothermia should raise suspicion of an overdose or CNS dysfunction due to infection or trauma. Table 20-2 Physiologic Changes Associated with Accidental Hypothermia
S B C Car Resp R Neur everity ody entral diovascula iratory enal omuscular Tempe Nervou r and rature s Endocr System ine M 3 L Tach Tach D Incre ild 5°C inear ycardia, ypnea, then iuresis; ased (95°F)– depressi then progressive increase preshiverin 32.2°C on of progressive decrease in in g muscle (90°F) cerebral bradycardia respiratory catechol tone, then metabol ; cardiac- minute amines, fatiguing ism; cycle volume; adrenal amnesia prolongatio declining steroids, ; n; oxygen triiodot apathy; vasoconstri consumptio hyronin dysarthr ction; n; e and ia; increase in bronchorrhe thyroxin impaire cardiac a; e; d output and bronchospa increase judgme blood in
nt; pressure sm metabol malada ism ptive with behavio shiverin r g M < E Prog Hypo 5 Hyp oderate 32.2°C EG ressive ventilation; 0% oreflexia; (90°F)– abnorm decrease in 50% increase diminishing 28°C alities; pulse and decrease in in renal shivering- (82.4°F progres cardiac carbon blood induced ) sive output; dioxide flow; thermogene depressi increased production renal sis; rigidity on of atrial and per 8°C autoreg level of ventricular drop in ulation conscio arrhythmias temperature intact; usness; ; suggestive ; absence of impaire pupillar (J- wave) protective d y ECG airway insulin dilatatio changes reflexes action n;
paradox ical undress ing; hallucin ations S < L Prog Pulm D No evere 28°C oss of ressive onic ecrease motion; (82.4°F cerebro decrease in congestion in renal decreased ) vascula blood and edema; blood nerve- r pressure, 75% flow conduction autoreg heart rate, decrease in parallels velocity; ulation; and cardiac oxygen decreas peripheral decline output; re- consumptio e in areflexia; in entrant n; apnea cardiac no corneal cerebral dysrhythmi output; or blood as; extreme oculocephal flow; maximum oliguria; ic reflexes coma; risk of poikilot loss of ventricular hermia;
ocular fibrillation; 80% reflexes asystole decreas ; e in progres basal sive metabol decreas ism e in EEG