Lecture 14: CV Control through Regulation of Cardiac Output Flashcards

1
Q

What is the role of CO and the importance of its regulation?

A
  1. Transport gases and substrates to and from organs and tissues at a rate commensurate with their requirements
    • match blood flow to requirements for total body, local organ and tissue
  2. excessive CO is nonproductive work!
  3. oxygen delivery is frequently sued as the cardiac output-defining parameter
    • not always the sole determinant of blood flow requirement (kidney, skin, GI tract)
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2
Q

What is the primary parameter that defines cardiac output?

A

Oxygen delivery

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3
Q

What is the primary parameter that matters for kidney in terms of cardiac output?

A

Volume rather than oxygen since it is used for filtration

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4
Q

What is the normal value range of CO?

A

Units = L/min
300 L/hr
7200L/day
200 x 10^6 liters in a lifetime

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5
Q

What is the cardiac index?

A

Cardiac output normalized to body size
L/min/m^2
Normal cardiac index (normalizes to body size): 2.5-3.5 L/min/m^2

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6
Q

What are the determinants of cardiac output?

A

No known sensors
Determined as a resultant of other inputs and reflexes such as
i. vascular resistance local metabolically mediated
ii. autonomic and neural inputs to the heart and vasculature
iii. local and central factors interact to determine global systemic vasculature resistance
Cardiac output is adjusted to maintain satisfactory arterial pressure

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7
Q

How do you measure cardiac output?

A
  1. By using the indicator dilution technique
    - fundamentally a conservation of mass expression
    - Addition of an indicator to a flowing stream produces a change in the indicator concentration downstream (therefore your measuring change in liters/min, ala units of CO)
    - The magnitude of the concentration change is related
    i. directly to the indicator addition rate
    ii. inversely to the stream flow rate
  2. Fick principle (oxygen as the indicator)
  3. Thermal dilution (heat as the indicator)
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8
Q

What is the fick cardiac output technique?

A

Oxygen is the indicator
May be considered as added to blood through lungs or removed as it passes through systemic circulation
CO = VO2/AVO2D
VO2 = total body oxygen consumption
AVO2D = change in arterial venous oxygen (amount of oxygen bound in Hb)

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9
Q

What are the characteristics of the thermal dilution technique?

A

Catheter with tip thermistor positioned in the main pulmonary artery
Injection of bolus of room T or iced saline in right atrium
Thermistor is cooled by injectate bolus as it is passed
CO may be calculated by integrating area under the time-temperature curve
-small area = high CO
-large area = low CO

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10
Q

What are the systemic venous O2 saturations?

A

Normal mixvenous O2 saturation is 75%
¼ of O2 transport capacity is actually utilized
Coronary sinus = 40%
Renal = 85%

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11
Q

What is the significance of mixed venous O2 saturation measures?

A

Mixed venous O2 measures the adequacy of cardiac output to meet metabolic requirements

  • useful clinical parameter easily measured with monitoring catheters
  • three-fold increase in metabolic requirements can be met without a change in CO
  • conditions with pathologically low cardiac output will have low mixed venous O2 saturation
  • *if it’s low, your patient is in trouble**
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12
Q

What is mixed venous oxygen saturation (SvO2)?

A

Percentage of oxygen bound to hemoglobin in blood returning to the right side of the heart

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13
Q

What are the components of the cardiac output?

A

CO = HR x SV
Heart rate can fluctuate at a 3-fold range (60-180)
SV is determined by preload, afterload, inotropic state, autonomic NS

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14
Q

What are the physiologic interactions that affect CO?

A

Increased heart rate = abbreviates diatolic filling tme so may reduce preload
Arterial pressure increases afterload and reduces ventricular ejection and stroke volume

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15
Q

What are the compensatory mechanisms for consequences of increased HR?

A

Most filling occurs during 1/3 of diastole so heart rates within the physiologic range do not impair diastolic filling

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16
Q

What are the compensatory mechanisms for consequences of increased arterial pressure?

A

Reduced ventricular ejection/stroke volume can be overcome by inotropic stimulation of normally function myocardium

17
Q

What is the impact of increasing CO?

A

Increasing HR and ventricular myocardial inotripic rate may be detrimental because of adverse impacts on myocardial metabolic supply/demand relationships, especially in cardiac disorders like CAD and valve disorders

18
Q

What is whipping the heart?

A

Increasing CO

Not good if you have some forms of heart disease

19
Q

What controls CO?

A

Principal determinant is local metabolic requirements
-increased local metabolic rate decreases local vascular resistance to match local flow to metabolic requirements
Leads to decrease in SVR and systemic arterial pressure
CV regulatory reflexes will compensate by restoring systemic arterial pressure to the normal range

20
Q

What are the modalities available to alter CO?

A
  1. Stroke volume
    i. preload
    ii. afterload
    iii. inotropy
  2. Heart rate
    i. autonomic input
21
Q

How can you alter preload to alter CO?

A

Control systemic venomotor tone

Control renal regulation of intravascular volume

22
Q

How can you alter afterload to alter CO?

A

Control SVR

23
Q

How does physical exercise regulate CO?

A
  1. increased skeletal muscle metabolic rate
  2. skeletal muscle vascular bed vasodilation
    -local factors and autonomically mediated
  3. decreased systemic arterial pressure and increased systemic venous return
  4. increased cardiac adrenergic input
    -increased HR and increased ventricular myocardial inotropic state
    Thus preload (venous return), afterload (decreasing SVR), inotropy and HR are all changed to increase CO
24
Q

What happens to CO during heat stress?

A

Increase cutaneous blood flow
Decrease vascular resistance to the skin and thus decrease in vascular resistance
Compensatory autonomic and vascular resistance mechanisms invoked to increase CO and restore vascular resistance

25
Q

What happens to CO in cold stress?

A

Cutaneous vasoconstriction to conserve heat (increase skin and global vascular resistance)
Increased arterial pressure
Decrease in systemic venous return
Decrease in preload = decrease in CO

26
Q

Why you don’t eat and run?

A

GI vasodilation to support digestive activity (decreased mesenteric vascular resistance)
Decreased arterial pressure
Blood diverted away from skeletal muscle
Increased CO as a result of decreased arterial pressure