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VETERINARY CLINICAL CARDIOLOGY
CARDIOLOGY CONCEPTS
Cardiovascular Physiology
The Determinants of Myocardial Performance
1. What are the determinants of myocardial performance?
These are the factors that affect the ability of the heart to contract effectively and they include:
  • Heart rate
  • Preload
  • Afterload
  • Contractility
  • Distensibility
  • Synergy of contraction
  • Involved in several of these factors is the concept of myocardial oxygen demand (MVO2).

    2. What is myocardial oxygen demand?
    This refers to the amount of oxygen required "demanded" of the heart to contract
    3. What factors affect MVO2?
    The following factors increase the myocardial oxygen requirement to contract:
    • An increase in heart rate.
    • An increase in contractility.
    • An increase in afterload.
    • An increase in wall stress

    Note the opposite changes in any of these factors reduces MVO2

    4. What is Wall Stress?
    Wall stress refers to the tension applied to a cross sectional area of muscle and the units are force per unit area. Laplace's Law is used to describe wall stress:

    Wall stress = (pressure x radius) divided by (2 x wall thickness).

    5. What is Stroke Volume?
    SV is the volume of blood ejected from the heart with each contraction. Under normal conditions only about 50% of the volume of blood present in the heart is ejected with each heart beat.
    6. What is Cardiac Output?
    CO is a commonly used measure of the performance of the heart.

    CO = Heart Rate x Stroke Volume.

    CO is sometimes indexed to body weight and is called cardiac index (CI = CO/Body Weight [kg])

    7. How does heart rate affect myocardial performance?
    An increase in HR increases CO and CI

    However an increase in HR:

    • increases MVO2
    • reduces the time for ventricular filling (preload)
    • reduces the time for coronary perfusion
    8. What factors affect heart rate?
    Under normal physiologic conditions heart rate is under autonomic control.
  • Sympathetic stimulation increases heart rate by increasing the rate of firing of the SA node.
  • Parasympathetic stimulation decreases heart rate by decreasing the rate of firing of the SA node.
  • The autonomic stimulation is influenced by:
    • Cephalic stimulation - excitement, boredom, sleeping, physical activity
    • Respiration: Hering-Brewer reflex. HR increases with inspiration and decreases with expiration. This rhythm is a sinus arrhythmia. During inspiration the reflex is stimulated to inhibit the vagal center resulting in a relative increase in sympathetic activity.
    • Baroreceptor activity: Involved in the minute to minute control of blood pressure which involves altering the tone on the arterial tree and altering heart rate. Any increase in BP activates the baroreceptors which stimulates the vasomotor center with increased vagal stimulation decreasing HR, decreasing CO, and returning BP to normal. Baroreceptors (or high pressure receptors) are located in the carotid sinus and aortic arch. These receptors respond to stretch and not pressure (thus mechanoreceptors). Activation of these receptors sends inhibitory impulses to the vasomotor center in the medulla of the brain via the vagus and glossopharyngeal nerves. The vasomotor center sends sympathetic nerve traffic to the body. Activation of the baroreceptor reflex inhibits sympathetic outflow and increases vagal tone. Reduced activation of these receptors, as with hypotension, increases sympathetic outflow (and thus HR) and inhibits vagal tone.
    • Other reflexes involved in HR control are:
      • Bainbridge Reflex: Increased left atrial pressure (due to increased volume) causes an increase in HR.
        • Mechanoreceptors located at the junction of the right atrium and caval veins or at the junctions of the pulmonary veins and the left atrium.
        • Volume expansion causes a tachycardia. Result is sometimes the opposite.
        • It serves as a counterbalance to the baroreceptor reflex.
        • Causes withdrawal of parasympathetic tone.

      Under abnormal/diseased conditions:

    • A number of disorders can induce either excessive heart rates (tachyarrhythmias) or excessively slow heart rates (bradyarrhythmias)
    9. How do baroreceptors affect cardiac function?

    Baroreceptor activity also affects the tone of arteries and veins and the contractility of the heart via activation or de-activation of the sympathetic and vagal output.

    Baroreceptor activity affects HR

    10. How might an abnormality of heart rate manifest?
    It may manifest as either:
  • An increase in HR - a tachyarrhythmia
  • A decrease in HR - a bradyarrhythmia
  • 11. What is preload?
    Preload refers to the volume of blood present in the heart at the end of diastole (before the onset of contraction).
    12. How is preload measured?
    Preload is measured as either the pressure in the ventricle at end diastole or the volume of blood in the ventricle at end diastole. Note that pressure and volume are intricately related
    13. How does preload affect myocardial performance?
    Preload alters cardiac performance by way of the Frank Starling Law of the heart.
    14. What is The Frank Starling Law of the heart?
    This law states that as preload is increased the contractility of the heart is increased to increase stroke volume.

    The mechanism for the action of the Frank Starling Law is as follows: the increased stretch of cardiac fibers at the onset of systole induces an increase in contractility by way of increasing the sensitivity of Tn-C for the existing amount of cytosolic Ca.

    15. What factors affect preload?
    Preload = volume of blood returning to the heart + the volume of blood left over from the last contraction (recall that approximately 50% of the blood in the ventricle is ejected during each contraction).

    Factors that increase preload:

    • Venoconstriction
    • Increased blood volume
    • Reduced ejection of blood from the ventricle due to reduced contractility so that more blood is left over at the end of the last contraction.
    • Increased blood volume due to valvular insufficiencies.

    Factors that reduce preload:

    • Venodilation
    • Blood loss with reduced circulating blood volume
    • An increase in the volume of blood ejected at the time of the last contraction
    16. How might an abnormality of preload manifest?
    If preload is too high? We usually observe signs of congestion.
  • The increase in volume and therefore pressure in the ventricle causes an increase in pressure in all the chambers and vessels that drain into the ventricle with the elevated preload.
    • If the ventricle is the left ventricle with the elevated preload, elevated pressures will develop in the left atrium, pulmonary veins, and pulmonary capillary bed and pulmonary arteries, right ventricle, right atrium, vena cavae, and veins that drain into the vena cavae. When the flux of fluid from the vasculature exceeds the ability of the lymphatics to accommodate then fluid accumulates.
      • The elevated hydrostatic pressure in the pulmonary capillary bed will promote the efflux of fluid into the pulmonary interstitium with pulmonary edema developing.
      • The elevated pressures in the right atrium will promote the collection of fluid in the pleural space (pleural effusion), in the abdominal cavity (ascites or abdominal effusion), or collection of fluid in the other organs such as the skin (subcutaneous edema) or edema of other organs.
    • If the ventricle is the right ventricle with the elevated preload, elevated pressures will develop in the right ventricle, right atrium, vena cavae, and veins that drain into the vena cavae.
      • The elevated pressures in the right atrium will promote the collection of fluid in the pleural space (pleural effusion), in the abdominal cavity (ascites or abdominal effusion), or collection of fluid in the other organs such as the skin (subcutaneous edema) or edema of other organs.

    If preload is too low? We observe signs of reduced blood volume or perfusion.

  • The reduction in volume and therefore pressure in the ventricle causes a reduced contractility (Frank Starling Law) and a reduced CO.
    • If the ventricle is the left ventricle with the reduced preload, hypotension will develop and reduced organ perfusion will occur with signs related to the organs involved.
    • If the ventricle is the right ventricle with the reduced preload, pulmonary artery hypotension will develop with reduced filling of the left heart and reduced organ perfusion will occur with signs related to the organs involved.
    17. How does the autonomic nervous system affect preload?
  • Sympathetic stimulation causes venoconstriction with increased venous return to the heart.
  • Reduction of venous stimulation or parasympathetic stimulation causes venodilation with reduced venous return to the heart.
  • 18. What is afterload?
    Afterload refers to the resistance the ventricle encounters as it tries to eject blood. Afterload is only conceptual and so it cannot be directly measured
    19. What factors affect afterload?
    Afterload is increased by:
    • An increase in ventricular volume
    • An increase in arterial vasomotor tone (arterial vascular resistance)
    • A decrease in ventricular wall thickness

    Afterload is decreased by:

    • A decrease in ventricular volume
    • A decrease in arterial vasomotor tone (arterial vascular resistance)
    • An increase in ventricular wall thickness

    Since arterial vasomotor tone is a strong component of afterload, blood pressure (BP) is frequently used as a surrogate for afterload, although a weak surrogate.

    20. What factors determine blood pressure?
    BP = CO x Arterial resistance

    Factors that influence systolic blood pressure:

    • Stroke Volume, Stiffness of the arterial tree, Arterial resistance

    Factors that influence diastolic blood pressure:

    • Duration of diastole, Elasticity in the arterial tree, Semilunar valve insufficiency, Arterial resistance
    21. What is pulse pressure?
    Pulse pressure refers to the difference between systolic BP and diastolic BP
    22. What is perfusion pressure?
  • Systemic perfusion pressure = Mean systemic BP - Central venous pressure (Right atrial pressure)
  • Pulmonary perfusion pressure = Mean pulmonary artery BP - mean pulmonary venous pressure
  • 23. What factors affect the physical examination assessment of systemic BP?
    BP cannot be directly assessed by physical examination. Palpation of the arterial pulse provides very indirect information as to BP but is usually inadequate.
    24. How is afterload measured?
    Afterload cannot be directly measured. However systemic arterial resistance can be measured but not without some difficulty? BP is a common surrogate used to assess afterload
    25. How does afterload affect myocardial performance?
    The effect of an increase in afterload is dependant on the inherent strength of the heart:
  • For a normal heart:
    • Very short term increases in afterload actually increase cardiac output.
    • More sustained increases in afterload result in a mild reduction in cardiac performance.
  • For a mildly depressed heart:
    • A moderate reduction in cardiac performance occurs with an increase in afterload.
  • For a heart with a severe reduction in contractility:
    • A profound reduction in stroke volume occurs with an increase in afterload.
    26. What factors determine arterial resistance?
    The factors that determine arterial resistance are explained in Poiseuille's Law:

  • Flow in a vessel is directly related to:
    • Change in pressure across the vessel
    • The radius of the vessel raised to the 4th power

  • Flow in a vessel is inversely related to:
    • The length of the vessel
    • Viscosity of blood (which is related to the # of red cells and protein content of the blood).

  • Recall: Flow = Pressure/Resistance
  • 27. How might an abnormality of afterload manifest?
    If afterload is too high:
    • Any disorder that causes a reduction in cardiac output will be associated with a "compensatory" increase in arterial vasomotor tone (systemic vascular resistance). Thus all cases of heart failure are associated with an increase in afterload.

    If afterload is too low:

    • Signs of a low BP may be observed

    Thus low BP may be observed with both an increase and decrease in afterload.

    28. How does the autonomic nervous system affect afterload?
    An increase in sympathetic tone increases afterload by increasing arterial resistance and increasing cardiac output via an increase in HR, preload (due to vasoconstriction) and Frank Starling's Law, and an increase in contractility. Reducing sympathetic tone will have the opposite effect.

    An increase in vagal tone will generally have the same effect as a decrease in sympathetic tone. A decrease in vagal tone will generally have the same effect as an increase in sympathetic tone.

    29. What is contractility?
    Refers to the inherent strength of the heart muscle - referred to as inotropy.
    30. What factors affect contractility?
    Factors that increase contractility:
    • Increased Beta adrenergic stimulation
    • Increase preload
    • Reduced vagal tone
    • Positive inotropic agents

    Factors that reduce contractility:

    • Reduced sympathetic stimulation
    • Reduced preload
    • Increased vagal tone
    • Negative inotropic agents
    31. How is contractility measured?
  • Cardiac ultrasound can directly measure contractility.
  • It can also be measured by MRI, or by pressure changes measured directly in the ventricle
  • 32. How does contractility affect myocardial performance?
    An increase in contractility results in:
    • An increase in stroke volume
    • A reduction in preload
    • An increase in MVO2

    A fall in contractility will have the opposite effects

    33. How might an abnormality of contractility manifest?
    If contractility is too high:
    • This condition will likely go undetected.

    If contractility is too low:

    • The resultant fall in BP will manifest as signs of hypotension
    • Fluid accumulation in the organs that drain into the weak ventricle
    34. How does the autonomic nervous system affect contractility?
  • The sympathetic nervous system increases contractility
  • The parasympathetic nervous system decreases contractility
  • 35. What is distensibility?
    Distensibility refers to the ease of ventricular filling during diastole (ability to stretch).

    Lusitropy refers to the ability of the ventricle to distend/relax and fill

    36. What factors affect distensibility?
    Distensibility is reduced by:
    • Reduced sympathetic tone
    • Increased wall thickness
    • Increased collagen, scarring, or cellular infiltration within the ventricular wall

    Distensibility is increased by the opposite effects.

    37. How is distensibility measured?
    Measurement of distensibility involves determining the instantaneous changes in pressure and volume within the chamber, which is invasive and difficult.

    Distensibility is not routinely measured.

    Indirect measures of the filling properties of the heart are obtained by echocardiography.

    38. How does distensibility affect myocardial performance?
    The effect of a reduction in distensibility is identical to the effect of an increase in preload. Thus, for the same volume of the heart at the end of diastole there will be an increase in pressure in the ventricle.
    39. How might an abnormality of distensibility manifest?
    If distensibility is reduced:
    • The clinical signs will be those of excessive preload with a reduction in SV

    If distensibility is excessive:

    • This is a situation not encountered in clinical practice.
    • Disease is characterized by a fall in distensibility
    40. How does the autonomic nervous system affect distensibility?
    Beta-adrenergic receptor activation increases the ability of the ventricle to relax
    41. What is synergy of contraction?
    Synergy of contraction refers to the normal harmonious, co-ordinated and efficient contraction of all regions of the heart yielding optimal ejection of fluid. Abnormalities of synergy of contraction are referred to as dyssynergy of contraction.
    42. How does dyssynergy of contraction affect myocardial performance?
    The mal-coordinated contraction of all regions of the heart result in reduced SV.
    43. How might an abnormality of synergy of contraction manifest?
    This disorder is the result of abnormal ventricular activation as with premature ventricular contractions.
    44. How might an abnormality of synergy of contraction be resolved?
    Therapy is directed as for that appropriate to treat ventricular dysrhythmias.
    45. How does the autonomic nervous system affect synergy of contraction?
    The sympathetic nervous system typically promotes ventricular dysrhythmias
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