D’YOUVILLE COLLEGE
BIOLOGY 307/607 - PATHOPHYSIOLOGY
Lecture 12 - CIRCULATORY SHOCK
1.
Circulatory Shock:
• normal blood flow: systemic blood pressure (BP) depends on balance of
adequate blood volume, appropriate cardiac output, & appropriate vascular
resistance
- cardiac output is governed by heart rate, & stroke volume (CO = HR x SV
= tissue blood flow); tissue blood flow relies upon BP that is sufficient to overcome
resistance to flow
- maintenance of adequate BP by negative feedback mechanisms was
discussed with cardiovascular physiology in chapter 10 (fig. 10 - 12 & ppt. 1)
- SV is governed by contractility (myocardial strength), by venous return
(preload = amount of filling = EDV), & by afterload (= factors that oppose flow);
normally, afterload is largely due to vascular resistance, which varies with vasodilation
(lowers resistance) or vasoconstriction (elevates resistance) (fig. 11 - 1 & ppt. 2)
• types of circulatory shock: shock occurs when BP is inadequate to support
normal tissue perfusion (fig. 11 - 2 & ppt. 3)
- primary (neurogenic) shock is a precipitous drop in BP that is usually
quickly corrected, e.g., by syncope (fig. 11 - 3 & ppt. 4); cardiogenic and vascular
components may contribute to this condition via signals from CNS (often instigated
Bio 307/607 lec 12
- p. 2 -
by emotional response that affects cardiovascular centers); may be more serious if
brain damage or drug induced alteration of neural activity is involved
Bio 307/607 lec 12
- p. 3 -
- cardiogenic shock is caused by failure of the heart to generate sufficient cardiac
output (= heart failure) (fig. 11 - 4 & ppt. 5); factors such as tamponade, muscular
weakness, disturbed electrical activity, pulmonary embolisms (low venous return),
may be involved (see fig. 10 - 26)
- vascular shock is caused by failure of the arterioles to produce sufficient
resistance to maintain BP (fig. 11 - 7 & ppt. 6); widespread vasodilation, causing
peripheral pooling of blood, may result from bacterial infection (septic shock), or
from a type I hypersensitivity (anaphylactic shock) (see fig. 5 - 14a & ppt. 7)
- hypovolemic shock is caused by factors that result in significant loss of blood
volume; blood loss (hemorrhagic shock), and fluid losses, e.g., from widespread
inflammations such as with severe burns are causes (fig. 11 - 5 & ppt. 8)
• compensatory mechanisms: negative feedback systems involve the brain
cardiovascular centers (fig. 11 - 8 & ppt. 9), or involve the kidney's reninangiotensin system (fig. 11 - 9 & ppt. 10) (also fig. 10 - 32 & ppt. 11)
- in severe ischemia of the brain, an intense sympathetic outflow is
generated (= CNS ischemic response)
• therapeutic interventions: blood or fluid replacements combat
hypovolemic shock
- vasoconstrictors combat vascular shock, but should not be used for
cardiogenic shock
- isoproterenol stimulates HR and contractility while promoting vasodilation,
actions that may alleviate cardiogenic shock
Bio 307/607 lec 12
- p. 4 -
• effects of shock: damage and dysfunction due to poor perfusion; lungs may
exhibit pulmonary edema, compromising respiratory function (adult respiratory
distress syndrome - ARDS)
- kidney failure - may produce acidosis, elevated toxins, reduced urine output
(fig. 11 - 10 & ppt. 12)
• stages of shock: nonprogressive shock may be readily alleviated by
compensations described above & therapeutic intervention
- progressive shock is more serious because of positive feedback effects
(fig. 11 - 11, 11 - 12 & ppts. 13 & 14); therapeutic interventions must be promptly
implemented
- irreversible shock: undeterred positive feedback that is lethal (fig. 11 - 13
& ppt. 15)