Page 242 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

"
increased sympathetic tone. Arterial vasocon- tration rate [GFR] < 15 mL/min, despite nor-
striction (not in shock caused by vascular dis- malization of blood pressure and volume), liv-
tension) directs the reduced cardiac output er failure (plasma bilirubin is elevated, pro-
away from the skin (pallor), the abdominal or- thrombin decreased), brain damage (loss of
gans, and the kidneys to vital organs (coronary consciousness, increasing degree of coma), dis-
arteries, the brain), bringing about centraliza- seminated intravascular coagulation, acute ul-
tion of the circulation. Vasoconstriction of the cers in the gastrointestinal tract with bleeding.
venous capacitance vessels (increased cardiac Several mechanisms are involved in shock,
filling), tachycardia, and positive inotropy, all some of them self-reinforcing.They aggravate
the result of sympathetic nervous activity, the shock until it can no longer be favorably in-
raise the previously reduced cardiac output fluenced, whatever the therapeutic measures
slightly. Epinephrine released from the adrenal (irreversible or refractory shock). The follow-
medulla supplements this nervous system ing vicious circles develop, among others:
mechanism.
1. Vasoconstriction ⇒ flow velocity ↓ ⇒
Heart and Circulation in blood pressure and arteriolar constriction 2a. Volume ↓ ⇒ blood pressure ↓ ⇒ peripheral
blood viscosity ↑ ⇒ flow resistance ↑ ⇒
! Volume compensation (→ A, right). The fall
flow velocity ↓↓ etc. until complete flow
arrest (stasis with sludge phenomenon)
with incipient shock diminishes the effective
(→ C1).
capillary filtration pressure, and thus intersti-
tial fluid flows into the blood compartment. In
vasoconstriction → hypoxia → arteriolar
addition, atrial pressure receptors recognize
spaces → volume ↓↓ ⇒ blood pressure ↓↓
which inhibits the secretion of atriopeptin
and reflexly brings about ADH secretion (Hen-
⇒ hypoxia ↑ (→ C2a).
7 the volume deficit (decreased atrial pressure), opening → fluid loss into interstitial
ry–Gauer reflex). ADH acts as a vasoconstrictor 2b.Volume ↓ ⇒ hypoxia ⇒ capillary damage
and to retain water. The reduction in renal ⇒ clot formation ⇒ disseminated intravas-
blood pressure increases the release of renin, cular coagulation ⇒ bleeding into tissues
more angiotensin II is formed, the latter stim- ⇒ volume ↓↓ (→ C2b).
ulating thirst and also having a vasoconstrictor 2 c. Hypoxia ⇒ capillary damage ⇒ thrombus
effect. In addition, it increases the secretion of formation ⇒ hypoxia ↑ (→ C2 c).
aldosterone, which in turn diminishes salt 3. Cardiac output ↓ ⇒ blood pressure ↓ ⇒
elimination, and thus water elimination, via coronary perfusion ↓ ⇒ myocardial hypox-
the kidney (→ p.122ff.). If the risk of shock ia ⇒ myocardial acidosis and ATP deficien-
can be averted, the lost erythrocytes will be re- cy ⇒ cardiac contractility ↓ ⇒ cardiac out-
placed later (raised renal erythropoietin forma- put ↓↓ (→ C3,4).
tion; → p. 30ff.) and the plasma proteins will 4a. Cardiac contractility ↓ ⇒ blood flow ↓ ⇒
be replenished in the liver by increased syn- thrombosis ⇒ pulmonary embolism ⇒
thesis. hypoxia ⇒ cardiac contractility ↓↓
If the organism is not able, without outside (→ C4a).
help (infusions etc.), to prevent the shock with 4b. Hypoxia ⇒ cardiac contractility ↓ ⇒ pul-
the above-mentioned homeostatic compensa- monary edema ⇒ hypoxia ↑ (→ C4b).
tory mechanisms, manifest (or decompensat- 4 c. Cardiac contractility ↓ ⇒ blood pressure ↓
ed) shock will develop (→ B). If the systolic ⇒ coronary perfusion ↓ ⇒ cardiac contrac-
blood pressure remains < 90 mmHg or the tility ↓↓ (C4 c).
mean pressure < 60 mmHg for a prolonged
period (which can happen despite volume re-
placement [protracted shock]), the consequen-
ces of hypoxia will lead to organ damage that
may culminate in extremely critical multior-
gan failure. Frequent organ damage includes
acute respiratory failure (= shock lung = adult
232 respiratory distress syndrome [ARDS]) with
hypoxemia, acute renal failure (glomerular fil-
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
All rights reserved. Usage subject to terms and conditions of license.