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VETERINARY CLINICAL CARDIOLOGY
CARDIOLOGY CONCEPTS
Cardiovascular Physiology
Compensation for Circulatory Failure
1. How does the cardiovascular system respond to failure?
So-called failure may be due to two causes:
  • Circulatory failure due to a lack of circulating volume usually due to blood loss and shock occurs.
  • A failure on the part of the heart to produce enough CO due to heart disease.
  • In both cases BP falls.

    All disorders that result in a fall in BP are addressed by "so-called compensation" on the part of the circulatory system as if the cause for this drop in BP was due to blood loss and reduced preload and the development of shock.

    2. What is the response of the circulatory system in the case of Shock?
    The response involves the following:
  • Activation/augmentation of the sympathetic nervous system causing:
    • An increase in HR - which increases CO
    • An increase in contractility - which increases SV
    • An increase in arterial vasomotor tone (systemic arterial resistance) - which helps bring BP back to normal
    • An increase in venomotor tone - which increases preload (the fundamental abnormality)
    • Activation of renin and thus RAAS
  • Activation of the Renin Angiotensin Aldosterone System (RAAS) causing:
    • The production of angiotensin II which causes:
      • An increase in arterial vasomotor tone (systemic arterial resistance) - which helps bring BP back to normal
      • An increase in venomotor tone - which increases preload (the fundamental abnormality)
      • Activates the Arginine Vasopressin (Antidiuretic) System that causes:
        • An increase in arterial vasomotor tone (systemic arterial resistance) - which helps bring BP back to normal
        • An increase in water retention at the level of the kidney - which increases preload (the fundamental abnormality)
    • The production of aldosterone which causes:
      • Water retention at the level of the kidney - which increases preload (the fundamental abnormality)
  • Increase thirst - which increases preload (the fundamental abnormality)
  • 3. Why is the shock response counter productive for cases of cardiac disease causing a fall in BP?

    The response the circulatory system introduces, for a true case of shock, is intended to support the circulatory system for a time period measured in hours.

    The so-called shock response was never intended to support a circulatory system in need of support for a time period measured from days to years.

    In the setting of heart failure that results in a fall in blood pressure, the "Shock Response" is activated for a period of days to years.

    4. How is the shock response counter-productive for cases of cardiac disease causing a fall in BP?
    How is sustained activation of the sympathetic nervous system detrimental?
  • The increase in HR causes an increase in MVO2, reduces the time for ventricular filling (diastole) and time for coronary perfusion.
  • The increase in contractility causes an increase in MVO2
  • The increase in arterial vasomotor tone (systemic arterial resistance) causes an increase in afterload which reduces SV and increases MVO2
  • The increase in venomotor tone - which increases preload promoting further pulmonary edema, pleural effusion, ascites, and organ edema
  • Activation of renin and thus RAAS as will be discussed is detrimental
  • Promotes arrhythmias - dyssynergy of contraction
  • Promotes coronary arterial spasm
  • Promotes myocardial necrosis
  • How is sustained activation of the RAAS detrimental?

  • The sustained production of angiotensin II is detrimental because:
    • The increase in arterial vasomotor tone (systemic arterial resistance) causes an increase in afterload which reduces SV and increases MVO2
    • The increase in venomotor tone - which increases preload promoting further pulmonary edema, pleural effusion, ascites, and organ edema
    • Myocardial necrosis
    • Activates the Arginine Vasopressin (Antidiuretic) System that causes:
      • An increase in arterial vasomotor tone (systemic arterial resistance) causes an increase in afterload which reduces SV and increases MVO2
      • An increase in water retention at the level of the kidney - which increases preload promoting further pulmonary edema, pleural effusion, ascites, and organ edema
  • The production of aldosterone which causes:
    • Water retention at the level of the kidney - which increases preload promoting further pulmonary edema, pleural effusion, ascites, and organ edema
    • Causes myocardial and vascular fibrosis

    Increased thirst is detrimental because it increases preload which promotes further pulmonary edema, pleural effusion, ascites, and organ edema

    Thus sustained activation of these "so-called compensatory" measures accelerates the demise of the patient with a dysfunctional heart as the cause for the reduction in BP. Thus activation of the shock response for a time period measured in hours is supportive. Activation of the shock response for a time period measured in days to years is detrimental.

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