Page 231 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

Circulatory Shock body during the non-progressive phase of
shock in order to ward off progressive shock
Shock is characterized by acute or subacute (! A). Rapid-acting mechanisms for raising the
progressive generalized failure of the circula- blood pressure and slower-acting mechanisms
tory system with disruption of the microcircu- to compensate for volume losses both play a
lation and failure to maintain adequate blood role.
flow to vital organs. In most cases, the cardiac Blood pressure compensation (! A left): A
output (CO) is insufficient due to a variety of drop in blood pressure increases sympathetic
reasons, which are explained below. tonus (! A1 and p. 214). Arterial vasoconstric-
! Hypovolemic shock is characterized by reduced tion (absent in shock due to vasodilatation)
central venous pressure and reduced venous return, shunts the reduced cardiac output from the
resulting in an inadequate stroke volume (Frank– skin (pallor), abdominal organs and kidneys
Starling mechanism). The blood volume can be re- (oliguria) to vital organs such as the coronary
Cardiovascular System betes mellitus, diabetes insipidus, high-dose diuretic striction of venous capacitance vessels (which
duced due to bleeding (hemorrhagic shock) or any
arteries and brain. This is known as centraliza-
other conditions associated with the external loss of
tion of blood flow (! A2). Sympathetic con-
fluids from the gastrointestinal tract (e.g., severe
vomiting, chronic diarrhea), the kidneys (e.g., in dia-
raises ventricular filling), tachycardia and
treatment) or the skin (burns, profuse sweating
positive inotropism increase the diminished
without fluid intake). An internal loss of blood can
cardiac output to a limited extent.
also occur, e.g., due to bleeding into soft tissues, into
Compensation for volume deficits (! A,
the mediastinum or into the pleural and abdominal
drop in blood pressure and peripheral vaso-
! Cardiogenic shock: Acute heart failure can be
8 space. right): When shock is imminent, the resultant
caused by acute myocardial infarction, acute decom- constriction lead to a reduction of capillary fil-
pensation of heart failure or impairment of cardiac tration pressure, allowing interstitial fluid to
filling, e.g. in pericardial tamponade. The central enter the bloodstream. Atrial stretch sensors
venous pressure is higher than in hypovolemic shock. detect the decrease in ECF volume (reduced
! Shock can occur due to hormonal causes, such atrial filling) and transmit signals to stop the
as adrenocortical insufficiency, diabetic coma or in- atria from secreting atriopeptin (= ANP) and to
sulin overdose (hypoglycemic shock). start the secretion of antidiuretic hormone
! Vasogenic shock: Reduced cardiac output can
also be due to peripheral vasodilatation (absence of (ADH) from the posterior lobe of the pituitary
pallor) and a resultant drop of venous return. This oc- (Gauer–Henry reflex; ! p. 170). ADH induces
curs in Gram-positive septicemia (septic shock), vasoconstriction (V 1 receptors) and fluid re-
anaphylactic shock, an immediate hypersensitivity re- tention (V 2 receptors). The drop in renal blood
action (food or drug allergy, insect bite/sting) in pressure triggers an increase in renin secretion
which vasoactive substances (e.g., histamines) are and activation of the renin–angiotensin–al-
released.
dosterone (RAA) system (! p. 184). If these
Symptoms. Hypovolemic and cardiovascular measures are successful in warding off the im-
shock are characterized by decreased blood pending shock, the lost red blood cells are later
pressure (weak pulse) increased heart rate, pal- replaced (via increased renal erythropoietin
lor with cold sweats (not observed with shock secretion, ! p. 88) and the plasma protein
caused by vasodilatation), reduced urinary concentration is normalized by increased he-
output (oliguria) and extreme thirst. patic synthesis.
Shock index. The ratio of pulse rate (beats/min) to Manifest (or progressive) shock will develop if
systolic blood pressure (mmHg), or shock index, pro- these homeostatic compensation mechanisms are
vides a rough estimate of the extent of volume loss. unable to prevent impending shock and the patient
An index of up to 0.5 indicates normal or ! 10% does not receive medical treatment (infusion, etc.).
blood loss; up to 1.0 = ! 20–30% blood loss and im- Severe hypotension (! 90 mmHg systolic or
pending shock; up to 1.5 = " 30–50% blood loss and ! 60 mmHg mean blood pressure) can persist for ex-
manifest shock.. tended periods, even in spite of volume replacement.
The resulting development of hypoxia leads to organ
218 Most of the symptoms described reflect the damage and multiple organ failure, ultimately
counterregulatory measures taken by the culminating in irreversible shock and death.
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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