co_regualtion lecture 9

Measurement of cardiac output by the Fick
-The Fick principle can be expressed by the following
Cardiac output = O2 Consumption / [02]pulmonary
vein -[02]pulmonary artery
-The equation can be solved as follows:
1. Oxygen consumption for the whole body can be
2. Pulmonary vein [02] can be measured in a
peripheral artery.
3. Pulmonary artery [02] can be measured in mixed
systemic venous blood.
-For example, a man has a resting O2 consumption
of 250 ml/min, a peripheral arterial O2 content
of 0.20 ml O2/ml of blood, and a mixed venous
O2 content
of 0.15 ml O2/ml of blood. What
is his cardiac output?
Cardiac output = 250 ml/min / (0.20 ml O2/ml- 0.15
ml O2/ml) = 5000 ml/min or 5.0 L/min (typical
value for a 70-kg male)
amount of stretch on the ventricular myocardium prior
to contraction
the arterial pressure (or some other measure of the
force) that a ventricle must overcome while it contracts
during ejection
Impedance/resistance to ventricular ejection
 Contractility
 myocardium’s intrinsic ability to efficiently contract
and empty the ventricle
 (independent of preload & afterload)
Determinants of Cardiac Output (CO)
Heart Rate
Contractility. This is a change in contractile energy of
the heart that is not due to changes in fibre length, but
rather to external factors such as SNS activity or drugs.
-is also called inotropism.
-can be estimated by the ejection fraction (stroke
volume / end-diastolic volume), which is normally
0.55 (55%).
-Agents that produce an increase in contractility
have a positive inotropic effect.
-Agents that produce a decrease in contractility
have a negative inotropic effect.
Factors that increase contractility (positive
inotropic effects)
a. Increased heart rate
-more action potentials per unit time ->Ca2 +
entry into the myocardial cell-> Ca2 + released
from the SR-> greater tension produced during
b. Sympathetic stimulation (catecholamines) via
beta1 receptors
c. Cardiac glycosides (digitalis)
-increase the strength of
contraction by inhibiting
Na+,K+ ATPase in the cardiac
muscle cell membrane
Factors that decrease contractility (negative
inotropic effects)
-Parasympathetic stimulation (ACh) via muscarinic
receptors decreases the strength of contraction in
atria by decreasing Ca2+ entry into the cell during
the plateau of the cardiac action potential (inward
Ca2+ current).
Changes in contractility shift the Frank-Starling
curve upward (increased contractility) or
downward (decreased contractility).
a. Increases in contractility cause an increase in cardiac
output for any level of venous pressure, right atrial
pressure, or end-diastolic volume.
b. Decreases in contractility cause a decrease in cardiac
output for any level of venous pressure, right atrial
pressure, or end-diastolic volume.
Increase in afterload decreases SV.
• High blood pressure: decreases SV
• Cholesterol: decreases SV(increases
• Obesity : decreases SV(increases
• Stress: decreases SV
• Exercise: increases SV
Afterload and Cardiac Performance
• Afterload: all the factors that impede fiber
shortening, in this case it would be all the
factors that impede the ejection of blood from
the ventricle. What the heart has to pump
Volume of blood in the arterial circulation
Pressure in aorta at onset of ejection (DAP)
Compliance of aorta
Size of outflow orifice
• The Diastolic Arterial Pressure (DAP) is the
major component that governs afterload in
the normal individual because it is the only
factor subject to moment to moment changes.
Conditions that Increase Afterload
• Hypertension
• Aortic stenosis
• Increased Hr
• In chronic pathological conditions these can lead to chronic
pressure overload of the heart
Myocardial Hypertrophy
• Cross sectional area of a muscle increases when repeatedly
exposed to an elevated work load over a sustained period of
• In cardiac muscle this can be the result of increased wall
tension caused by increased preload, increased afterload or
increased heart rate.
• Some hormones have also been implicated in the process
• Norepi, angiotensin II, and thyroxin
Three Types of Hypertrophy
1) Physiological – occurs in athletes in response to long term
endurance exercise.
there is a symmetrical enlargement
2) Concentric – occurs as a result of long standing pressure
overload. Thickness ratio is increased, ventricle lumen size can
be unchanged or reduced.
3) Eccentric – occurs as a result of long standing volume
overload. Hypertrophies away from lumen, enlarging lumen
size and the thickness ratio is reduced.
Swollen legs
A 47 year old woman was brought to the hospital because of severe shortness of
breath and swelling of her lower body. Over the last year *she had noticed periods
of shortness of breath while doing her housework (exertional dyspnea). She also
had shortness of breath while lying down (orthopnea). The patient often awoke at
night with a sensation of not getting enough air and she had to sit or stand to
obtain relief (paroxysmal nocturnal dyspnea). #More recently she noticed swelling
first of her lower extremities and then of her lower abdomen. The swelling was
worse through the day and decreased overnight. She reported awakening three to
four times a night to urinate. The patient did not remember any ill health before
these problems began.
Physical examination revealed a woman sitting up in bed in mild to moderate
respiratory distress. Her blood pressure was 100/70, pulse was 120 and weak.
Respirations were 26 per minute and labored. There was jugular venous
distension, even while she was sitting. Palpation of the sternum revealed a
restrosternal lift. Auscultation of the heart revealed an opening snap and a long
diastolic rumble at the apex. Auscultation of the lungs revealed crackles halfway
up the lungs. There was also severe lower extremity edema.
During her hospitalization, as part the work-up, the following studies were done.
O2 consumption(VO2)
Arterial-venous O2 content
Heart rate
Mean Pulmonary Capillary Wedge
Right Ventricular Systolic pressure
End-Diastolic pressure
Right Ventricular End Diastolic
188 ml/min
5.3 ml/dl blood
3.0-5.0 ml/dl blood
25 mm Hg
60-100 beats/min
<15 mmHg
80 mm Hg
16 mm Hg
140 ml/m2
•Use the data in the table above to calculate cardiac output and ejection fraction
· Evaluate the mean electrical axis of the heart using the ECG shown overleaf
C. Regulation of CO and Venous Return (VR)
“ VR determines CO”, but since VR is not an
independent variable, and is largely determined
by Central Venous Pressure (CVP), so it is more
accurate to say that CVP determines CO
• CVP is affected by blood volume (BV),
vasoconstriction and arteriolar vasoconstriction
. When VR becomes higher than the heart can
pump (e.g. exercise), then the contractility of the
heart is adjusted () by SNS, so that CO is
matched to the VR
Quantitative Analysis of CO Regulation
Two primary factors are related to CO regulation: 1. The
pumping ability of the heart (represented by CO curves
that we discussed); and 2. The factors that affect CVP, and
consequently VR. These are represented by the vascular
function curves (also known as the venous return curves)
Vascular Function Curves:
- VR is determined by P between central veins and the
right atrium. The grater P the larger VR and vice versa
- The lower the pressure in RA, the greater the pressure
gradient between the veins and RA, and vice versa (as
RAP, VR )
Fig. 10. A typical Vascular Function Curve
Mean Systemic Filling Pressure (MSFP)
-The graph shows that as RAP, VR. The slope is very steep, and
this is due to the fact that veins are very compliant (distensible)
- When RAP is ~7 mm Hg, the VR is zero, i.e. there is no pressure
gradient between RA and the veins to drive the blood back to the
heart. This pressure is referred to as mean systemic filling pressure
- The value of MSFP is 7 mm Hg and not zero because it depends
on the volume of blood in the vascular system and its overall
- The overall distensibility or compliance of vascular system
depends on the degree of venomotor tone as well as artriolar tone
- The factors affectingg MSFP are: Blood volume, Venomotor tone,
Arteriolar resistance

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