Hypertensive- Shock 2 Flashcards Preview

Term 5 - PathoPhysio > Hypertensive- Shock 2 > Flashcards

Flashcards in Hypertensive- Shock 2 Deck (15):

The causes and types of shock:

  1. Hypovolemic shock:
    • Inadequate volume of blood to fill the vascular system
  2. Distributive shock (also called vasogenic or low-resistance shock):
    • Increased size of the vascular system produced by vasodilation in the presence of a normal blood volume
  3. Cardiogenic shock:
    • Inadequate output of the heart as a result of myocardial abnormalities
  4. Obstructive shock:
    • Inadequate cardiac output as a result of obstruction of blood flow in the lungs or heart


Physical findings in Hypovolemic Shock:

  • Hypotension (systolic pressure <90)
  • A rapid, low volume, thready pulse
  • Cold, pale, clammy skin
  • Intense thirst
  • Rapid respiration
  • Restlessness or Low activity
  • Markedly decreased urine output
  • Altered mental status
  • Do not rely on systolic BP as the main indicator of shock. Compensatory mechanisms prevent a significant decrease in systolic BP until the patient has lost 30% of the blood volume


Compensatory reactions activated by Hypovolemic Shock:

  • Vasoconstriction & consequences
  • Tachycardia
  • Venoconstriction
  • Tachypnea – cause and benefit
  • Increased movement of interstitial fluid into capillaries
  • Increased secretion of ADH
  • Increased secretion of glucocorticoids
  • Stimulation of renin-angiotensin-aldosterone
  • Increased secretion of erythropoietin
  • Increased synthesis of plasma proteins


Hypovolemic shock:

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Hypovolemic shock:

Baroreceptor response to decrease in BP


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  • Hypovolemic shock:
  • Compensatory Mechanisms
  • Neurohormonal Activation

  • Angiotensin II
  • Epinephrine
  • Norepinephrine
  • Vasopressin (ADH)
  • ACTH
  • Aldosterone


Hypovolemic shock:

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Consequences of increased vasomotor discharge during hypovolemic shock:

  1. Vasoconstriction is generalized, sparing only the vessels of the brain and the heart
  2. Vasoconstriction in the skin - Coolness and pallor
  3. Vasoconstriction in the kidney – Drop in GFR. This reduces water loss, but it reaches a point at which nitrogenous products of metabolism accumulate in the blood (prerenal azotemia). If hypotension is prolonged, there may be severe renal tubular damage, leading to acute renal failure.


Reason for tachypnea and its importance in hypovolemia:

  • The fall in blood pressure and the loss of red cells results in stimulation of the carotid and aortic chemoreceptors → stimulation of respiratory center→ Chemoreceptor reflex
  • Stimulation of respiration increases thoracic pumping and improves venous return
  • Stimulation of respiration also increases vasoconstrictor discharge


Hypovolemic shock:

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Hypovolemic shock:

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Hypovolemic shock:

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Hypovolemic shock:

Refractory Shock:

  • The shock persists for hours and eventually reaches a state in which there is no longer any response to vasopressor drugs
  • Even if the blood volume is returned to normal, cardiac output remains depressed
  • Factors that make shock refractory are:
    • Precapillary sphincters are constricted for several hours but then relax while postcapillary venules remain constricted. Therefore, blood flows into the capillaries and remains there.
    • Cerebral ischemia depresses vasomotor and cardiac discharge, causing blood pressure to fall and making the shock worse.
    • Reduced myocardial blood flow.


Traumatic Hypovolemic Shock:

  • Traumatic shock involves severe damage to muscle and bone - as seen in battle casualties and automobile accident victims
  • Significant bleeding into the injured areas
  • Breakdown of skeletal muscle is a serious additional problem when shock is accompanied by extensive crushing of muscle (crush syndrome)
  • Free radicals generated at the sites cause further tissue destruction (reperfusion-induced injury)
  • Increased Ca 2+ in damaged cells can reach toxic levels
  • Large amounts of K+ enter the circulation
  • Myoglobinuria worsens renal failure


Hypovolemic shock:

A complication of shock that has a very high mortality rate is:

  • Pulmonary damage with production of acute respiratory distress syndrome (ARDS)
  • The cause for ARDS: Capillary endothelial cell damage and damage to alveolar epithelial cells with the release of cytokines