Cardiac Output Tutorial and Concept Map

1
Cardiac Output Tutorialand Concept Map

• J. Ellen Lathrop-Davis
• Community College of
• Baltimore County, MD

2
Cardiac Output is

• the volume of blood that leaves each ventricle
  during each minute
• measured in milliliters (mL) per minute (min) or
  liters (L) per minute
• normally around 5,000 mL (5 L) per minute (5,000
  mL/min or 5 L/min)

3

• Cardiac output (CO) is directly affected by
• heart rate (HR), the number of times the heart
  beats each minute and
• stroke volume (SV), the amount of blood ejected
  during each beat

CO HR x SV

• If HR increases, what will happen to cardiac
  output?
• If SV decreases, what will happen to cardiac
  output?

4

• Heart Rate is directly affected by factors called
  chronotropic agents (or factors).
• These factors may be positive or negative.

5

• Positive chronotropic agents
• increase heart rate and
• include epinephrine, norepinephrine and beta
  agonists (e.g., isoproterenol).

• What effect will sympathetic nerve impulses have
  on heart rate?

6

• Negative chronotropic agents
• decrease heart rate and
• include acetylcholine (ACh) and beta antagonists
  (e.g., propranolol).

• What effect will parasympathetic nerve impulses
  have on heart rate?

7

• Stroke Volume is affected by
• preload,
• contractility and
• afterload

• What effect will increased preload or increased
  contractility have on stroke volume?

8

• Preload
• is the volume-dependent pressure exerted on the
  walls of the ventricles by the blood in them at
  the end of diastole (end diastolic volume EDV)
  and
• stretches the myocardium so that the myofibers
  are lengthened before contraction resulting in a
  stronger contraction, up to a point (above which
  strength decreases), according to the
  Frank-Starling law of the heart.

9

• Preload is directly affected by
• filling time and
• venous return

10

• Filling time is inversely related to heart rate
  as heart rate increases, filling time decreases.
• Chronotropic agents affect filling time, thus
  they affect EDV. However, these agents may also
  affect contractility such that the effects on
  stroke volume are less straightforward.

• What effect will increased heart rate have on
  stroke volume (if other factors stay the same)?

11

• Venous return depends on how much blood returns
  to the heart, which is affected by
• blood volume,
• venous pressure and
• intrathoracic pressure

• What effect will increased venous return have on
  EDV?

12

• Blood volume and venous pressure (which
  increases during venoconstriction constriction
  of the veins) directly affect venous return.

• What effect will blood loss have on EDV?

13

• Intrathoracic pressure (which decreases during
  inspiration and increases during expiration)
  inversely affects venous return.

• What effect will inhaling more deeply have on
  venous return?

14

• Contractility is
• the ability to generate tension independent of
  the effects of preload and afterload
• affected by factors called inotropic agents

15

• Positive inotropic agents
• increase contractility and
• epinephrine, norepinephrine and cardiac
  glycosides (e.g., digitalis)

• What effect will epinephrine have on stroke
  volume?

16

• Negative inotropic agents
• decrease contractility and
• include calcium channel blockers (e.g.,
  verapamil).

• What effect will blocking calcium channels have
  on stroke volume?

17

• Afterload is
• the amount of tension the ventricles need to
  generate in order to eject blood into the
  arteries
• directly affected by arterial blood pressure

• What effect will hypertension have on afterload?

18

• Afterload
• inversely affects stroke volume and
• directly affects the volume of blood left in the
  ventricles at the end of systole (end systolic
  volume ESV)

• What effect will hypertension have on stroke
  volume?

19
In Summary

• Heart rate and stroke volume are the two factors
  that determine cardiac output.
• Each of these is affected by many factors.
• Chronotropic agents affect heart rate while
  inotropic agents affect contractility, which
  affects stroke volume.
• Some factors (e.g., epinephrine and
  norepinephrine) affect both.

20
Cardiac Output Concept Map
21
Answers to Questions

• If HR increases, what will happen to cardiac
  output? Cardiac output increases.
• If SV decreases, what will happen to cardiac
  output? Cardiac output is expected to decrease
  (note that heart rate can be increased to
  compensate).
• What effect will sympathetic nerve impulses have
  on heart rate? The norepinephrine released will
  increase heart rate.
• What effect will parasympathetic nerve impulses
  have on heart rate? The ACh released will
  decrease heart rate.

22
Answers to Questions

• What effect will increased heart rate have on
  stroke volume (if other factors stay the same)?
  Stroke volume will decrease (note that SV may be
  maintained if the cause of the increased heart
  rate also increases contractility).
• What effect will increased venous return have on
  EDV? EDV will increase.
• What effect will blood loss have on EDV? EDV
  will decrease (note that the body has
  compensatory mechanisms to initially maintain SV
  when blood is lost).

23
Answers to Questions

• What effect will inhaling more deeply have on
  venous return? Venous return will increase
  because deeper inhalation lowers thoracic
  pressure more than normal.
• What effect will epinephrine have on stroke
  volume? Stroke volume will increase due to the
  increased contractility.

24
Answers to Questions

• What effect will blocking calcium channels have
  on stroke volume? Stroke volume will decrease.
• What effect will hypertension have on afterload?
  Afterload will increase.
• What effect will hypertension have on stroke
  volume? Stroke volume will decrease (and the
  heart will have to work harder to eject blood).