Oxygen consumption (by spirometer) (VO2)

The principle can be used to determine cardiac output by

measuring the amount of oxygen consumed by the body in a given period
dividing this value by the A-V difference across the lung.
Because systemic arterial blood has the same oxygen content in all parts of the body, the arterial
oxygen content can be measured in a sample obtained from any convenient artery.
A sample of venous blood in the pulmonary artery obtained by means of a cardiac catheter.
Right atrial blood has been used in the past, but mixing of this blood may be incomplete, so that the
sample is not representative of the whole body.
Output of left ventricle= {250 mL/min} / {[190mL/L arterial blood] – [140mL/L venous blood]}
2. Indicator dilution method:
A second technique is a variation on the Fick method.
A known quantity of a dye is injected into the right atrium via catheter.
Small amounts of blood are continuously withdrawn from the arterial system with an indwelling
catheter and passed through a photosensitive device that measures dye concentration.
The resulting curve measures dye concentration as a function of time.
The area under the dye-dilution curve can be calculated and approximates the average
concentration of dye over time. Knowing the quantity of dye injected, the cardiac output can be
determined by:
Cardiac output = Quantity of dye injected ÷ area under the curve
3. Thermo-dilution method:
The indicator used is cold saline.
The cold saline is injected into the right atrium through one side of a double-lumen catheter, and the
temperature change in the blood is recorded in the pulmonary artery, using a thermistor in the other,
longer side of the catheter. The temperature change is inversely proportionate to the amount of
blood flowing through the pulmonary artery, i.e., to the extent that the cold saline is diluted by blood.
This technique has two important advantages.
The saline is completely innocuous ‫غير مؤذي‬.
The cold is dissipated‫ تتبدد‬in the tissue, so recirculation is not a problem
 it is easy to make repeated determination.
4. Doppler technique with echocardiograph:
Factors Affection stroke volume:
The systolic performance of the heart is determined by 3 factors: preload, afterload, and contractility.
1. Preload ‫مقدار الشد او الحمل الذي يتحمله البطين بسبب الدم الراجع عندما يكون البطين في حالة ارتخاء‬
Preload is passive tension or load on the ventricular muscle in the relax state
Preload is a passive tension on ventricular muscle when it is being filled with blood at the end of diastole
Preload on ventricular muscle is not directly but indirectly. Preload is determined by:
A. Left ventricular preload:
 left ventricular end diastolic volume and left ventricular end diastolic pressure.
 less reliable: left atrial pressure, pulmonary venous pressure, pulmonary wedge pressure)
B. Right ventricular preload: systemic central venous pressure
venous return
atrial contraction.
Venous return is the quantity of blood flowing from veins
into the right atrium each minute. ‫كمية الدم االراجعة للقلب من االوردة‬
The venous return = the cardiac output.
Venous return is the quantity of blood flowing from veins into the right atrium each minute.
The sum of all local tissue blood flow will determine the venous return which will determine
cardiac output.
This why increasing level of work output during exercise, oxygen consumption and cardiac
output increase in parallel to each other.
Hemodynamically, venous return (VR) to the heart from the venous vascular beds is
determined by a pressure gradient (venous pressure, PV, minus right atrial pressure, PRA)
divided by the venous vascular resistance (RV)
Venous return =
(𝐯𝐞𝐧𝐨𝐮𝐬 𝐩𝐫𝐞𝐬𝐬𝐮𝐫𝐞( 𝐏𝐕) 𝐦𝐢𝐧𝐮𝐬 𝐫𝐢𝐠𝐡𝐭 𝐚𝐭𝐫𝐢𝐚𝐥 𝐩𝐫𝐞𝐬𝐬𝐮𝐫𝐞( 𝐏𝐑𝐀)
𝐯𝐞𝐧𝐨𝐮𝐬 𝐯𝐚𝐬𝐜𝐮𝐥𝐚𝐫 𝐫𝐞𝐬𝐢𝐬𝐭𝐚𝐧𝐜𝐞 (𝐑𝐕)
Three principal factors that affect venous return to the heart from the systemic circulation:
1. venous pressure (PV) in peripheral veins (when the body is supine) is only a few mmHg
higher than right atrial pressure.
Venous pressure is measured by mean systemic filling pressure this is the pressure
measured everywhere in the systemic circulation when all flow of blood is stopped. It is the
forces the systemic blood toward the heart
2. Right atrial pressure, which exerts a backward force on the veins to impede flow of blood
from the veins into the right atrium.
Right atrial pressure (PRA): is normally very low (fluctuating a few mmHg around a mean of 0
mmHg).
The pressure gradient (mean systemic filling pressure minus Right atrial pressure) driving
venous return from peripheral veins to the heart is relatively low (<10 mmHg)
↓ Right atrial pressure → ↑ ΔP → ↑ venous return (reverse is true)
↑ mean systemic filling pressure → ↑ ΔP → ↑ venous return (reverse is true)
For example, during lung expansion,
a. Right atrial pressure can transiently fall by several mmHg.
b. Venous pressure in the abdominal compartment may increase by a few mmHg.
These changes result in a large increase in the pressure gradient driving venous return from
the peripheral circulation to the right atrium.
3. Resistance to blood flow between the peripheral vessels and the right atrium.
The variable is most significant in determining venous return is venous resistance because in
steady state, right atrial pressure is usually 0 and mean systemic pressure is usually kept
constant.
Because venous return is equal to cardiac output so
𝑴𝒆𝒂𝒏 𝒂𝒓𝒕𝒆𝒓𝒊𝒂𝒍 𝒑𝒓𝒆𝒔𝒔𝒖𝒓𝒆 𝒎𝒊𝒏𝒖𝒔 𝑹𝒊𝒈𝒉𝒕 𝒂𝒕𝒓𝒊𝒂𝒍 𝒑𝒓𝒆𝒔𝒔𝒖𝒓𝒆
Cardiac output=
𝑻𝒐𝒕𝒂𝒍 𝒂𝒓𝒕𝒆𝒓𝒊𝒂𝒍 𝒓𝒆𝒔𝒊𝒔𝒕𝒂𝒏𝒄𝒆
The factors that aid for venous return are:
Muscle pump (Rhythmical contraction of limb muscles):
normal locomotory activity (walking, running, swimming)
promotes venous return.
Veins physically located within large muscle groups undergo
compression as the muscles surrounding them contract. Veins
become decompressed as the muscles relax. Therefore, with
normal cycles of contraction and relaxation, the veins are
alternately compressed and decompressed (i.e., "pumped").
In Large Veins one-way valves spaced at 2-4 cm intervals so
permit blood to move forward towards the heart & prevent the
backflow. Since the venous valves prevent reverse flow, the
blood moves toward the heart (i.e., enhances venous return).
When a person is standing, postural muscles in the legs
alternately contract and relax to keep the body in balance.
This muscle activity
a. promotes venous return.
b. helps to maintain central venous pressure and venous return,
c. lower venous and capillary pressure in the feet and lower
limbs because the pressure in leg increase during standing.
 Heartbeat:
A. Vis-a-Tergo ‫(القوة الخلفية‬force acting on venous return from behind):
The contraction of the left ventricle creates a pressure that pushes blood from behind all along the
vascular tree throughout the body.
B. Vis-a-Fronte ‫(القوة االمامية‬force acting on venous return from front):
The pressure in the right atrium is normally around 0 mm Hg.
Causes of negative pressure in right atrium
a. During ventricular contraction, the atrioventricular ring is pulled down. As a result of this, the atria
get expanded.
b. during sudden rush of blood from atria to ventricle.
These two negative pressures exerts suction effect on the great veins and draws blood into the
atrium.
Abdominal Pump:
Normally, veins present in the splanchnic region act as reservoir for blood.
When the abdominal muscles contract→↑intra-abdominal pressure →compression of veins occurs
in the abdominal region→↑ venous return by increasing the gradient towards the thoracic cavity
(heart).
Decreased venous compliance.
Sympathetic activation of veins →venoconstriction + ↓ venous compliance→ ↑ venous pressure →
↑venous return
 Respiratory Activity (Abdomino-thoracic or Respiratory Pump)
A. Right side of the heart
Inspiration ►the chest wall expands, and the diaphragm descends ► intra-pleural pressure
become more negative ►a. expansion of the lungs + b. fall of intra-cardiac pressures
→↓right atrium pressure + ↓ thoracic superior and inferior vena cava pressure → ↑the
pressure difference between mean venous pressure and right atrial pressure → ↑venous
return
During expiration, the opposite occurs.
B. Left side of the heart
During inspiration, expansion of the lungs and pulmonary tissues →↑ pulmonary blood
volume → transiently decreases the flow of blood from the lungs to the left atrium.
‫ينحصر الدم ب الرئة‬Therefore, left ventricular filling actually decreases during inspiration.
During expiration, the reverse occurs.
Increasing the rate and depth of respiration promotes venous return and therefore enhances
cardiac output.
Non-typical respiratory activity such as doing a forced expiration against a closed glottis
(Valsalva maneuver) impedes and therefore reduces venous return and cardiac output.
Vena cava compression.
An increase in the resistance of the vena cava, as occurs when the thoracic vena
cava becomes compressed during a Valsalva maneuver or during late
pregnancy, decreases venous return due to increase venous resistance
 Gravity.
The effects of gravity on venous return seem paradoxical
Theoretically, when a person stands up hydrostatic forces → ↓ the right atrial
pressure + ↑the venous pressure in the dependent limbs →↑the pressure
gradient →↑ venous return
Actually, when a person stands venous return decreases.
Standing up (not exercising) there will be no pumping activity of the muscle →↓
venous return→↓preload→↓cardiac output→↓blood pressure
Abnormalities that decrease venous return (factors affect venous return):
1. Decreased blood volume.
Loss of blood decreases often from hemorrhage

the filling of the vascular system to such a low level that there is not enough blood in the peripheral vessels to create
peripheral vascular pressures (i.e., decrease venous pressure)high enough to push the blood back to the heart.

Decrease venous return.
2. Acute venous dilation.
when the sympathetic nervous system suddenly becomes inactive or use vasodilators (as Nitroglycerin)

flaccid peripheral blood vessels + Acute venous dilation.

decreases the filling pressure of the vascular system.

Decrease venous return+ fainting.
3. Obstruction of the large veins.
the large veins leading into the heart become obstructed as Inferior vena cava obstruction during pregnancy or due to
Valsalva maneuver.

Decrease venous return.
4. Decreased tissue mass, especially decreased skeletal muscle mass.
With normal aging or with prolonged periods of physical inactivity.

a reduction in the size of the skeletal muscles usually occurs.

decreases the total oxygen consumption and blood flow needs of the muscles.

decreases in skeletal muscle blood flow.

Decrease venous return.
5. Decreased metabolic rate of the tissues.
↓ tissue metabolic rate is reduced (skeletal muscle during prolonged bed rest or hypothyroidism)

↓the oxygen consumption and nutrition needs of the tissues.

↓ blood flow to the tissues.

Decrease venous return.
Regardless of the cause of low cardiac output, whether it is a peripheral factor or a cardiac factor, if ever the
cardiac output falls below the level required for adequate nutrition of the tissues, the person is said to be
experience circulatory shock.
Frank-Starling relationship:
The Frank-Starling law of the heart (also known as Starling's law or the Frank-
Starling mechanism or Maestrini heart's law) states that
"Within physiological limits, the force (or strength) of ventricular contraction is directly proportional to
the initial length of the muscle fiber (end diastolic volume), which an intrinsic property of myocardium
‫) وهي خاصية موروثة‬end diastolic volume( ‫ضمن الحدود الفسلجية مقدار قوة تقلص البطين يتناسب طرديا مع مقدار طول الليف العضلي للبطين‬
“Energy of contraction is proportional to the initial energy of cardiac muscle fibers”.
↑ end diastolic volume →↑ stretch of myocardium → ↑number of interactions between actin and
myosin→↑ force of contraction →↑ stroke volume).
The Frank-Starling mechanism is extremely
important in balancing the output of the two sides
of the heart over extended periods.
Then the stroke volume of the heart increases in
response to an increase in the volume of blood
filling the heart (the end diastolic volume or venous
return or pre-load) when all other factors remain
constant.
increase preload causes:
A. length-tension relation:
the length tension relationship is controlled by
a. total tension: tension develop If the muscle is stimulated to contract under isometric
conditions (fixed length) caused by the contractile element of myocardium
b. passive tension caused by the elastic element of myocardium
c. active tension equal total tension minus the resting tension
The length-tension diagram shows that as preload increases, there is an increase in
active tension up to a maximal limit.
 at low resting sarcomere lengths 1.6μ (i.e., at low preloads), the amount of active
tension developed is relatively small.
at high resting sarcomere lengths 1.9μ (i.e., at high preloads), the amount of active
tension developed is relatively high.
The maximal active tension corresponds in cardiac muscle to a sarcomere length
of about 2.2 microns. Cardiac muscle, unlike skeletal muscle, does not display a
descending limb on the active tension curved because the greater stiffness of cardiac
muscle normally prevents its sarcomeres from being stretched beyond 2.2 microns.
The changes in active tension caused by :
 changes in preload are related to changes in the number of actin and myosin
cross bridges formed, which depends on the sarcomere length.
Changes in preload also affect active tension by altering the sensitivity of troponin
C to calcium.
↑ venous return→ ↑ stretch of cardio-myocyte sarcomeres (length-dependent
activation) → ↑altered calcium handling and troponin C affinity for calcium
→↑increased of cross-bridges in actin/myosin myo-filaments →↑ force of
contraction.
According to above Preload can be defined as
 is the initial stretching of the cardiac myocytes prior to contraction and
 is related to the sarcomere length.
B. force-velocity relation
there is an inverse relationship between velocity of shorting and force generated during shorting
(afterload or tension)
Fmax represents the point at which the afterload is so great that the muscle fiber cannot shorten,
and therefore represents the maximal isometric force.
Vmax represents the point at which there were no afterload that the muscle fiber has maximal
velocity of shortening.
Effect of increase preload (‫اي نسمح للدم ان يدخل‬with constant after load ‫اي النسمح للدم ان يخرج‬
a. increases the maximal isometric force (Fmax), Point A, B, C; but does not alter (Vmax).
b. increase velocity of contraction; Point I, 2, 3.
Stretching the heart causes the heart to pump faster, resulting in an increased heart rate by:
Stretch of the sinus node in the wall of the right atrium has a direct effect on the
rhythmicity of the node to increase the heart rate as much as 10 to 15 percent.
The stretched right atrium initiates a nervous reflex called the Bainbridge reflex also to
increase the heart rate.
Ventricular filling and therefore preload is increased by:
Increased central venous pressure that can result from
a. decreased venous compliance (i.e., Increase venous tone) e.g., caused by sympathetic
activation of venous smooth muscle.
b. increased thoracic blood volume, which can be increased by
i. increased total blood volume.
ii. increase venous return which can be augmented by
1. increased respiratory activity (e.g., Increase negative intra-thoracic pressure)
2. increase pumping action of skeletal muscle.
3. decrease effects gravity (e.g., head-down tilt).
Increased ventricular compliance, which results in a greater expansion of the
chamber during filling at a given filling pressure.
Increased atrial force of contraction resulting from
a. sympathetic stimulation of the atria
b. increased filling of the atria
therefore, increased atrial contractile force →↑ preload
Reduced heart rate, which increases ventricular filling time.
Increased aortic pressure (i.e., ↑ afterload on the ventricle) →↓ stroke volume
+ ↑ end-systolic volume → secondary increase in ventricular preload.
Pathological conditions such as
a. ventricular systolic failure
b. valve defects such as :
Left ventricular preload : aortic valve stenosis, and regurgitation.
Right ventricular preload: pulmonary valve stenosis and regurgitation.
several non-pathological states may result in increased preload. These
include: (Pregnancy, Exercise, Excessive sodium intake, Intravenous fluid)
Ventricular preload is decreased by:
Decreased venous blood pressure, most commonly resulting from
a. reduced blood volume (e.g., hemorrhage)
b. gravity causing blood to pool in the lower limbs when standing upright.
c. increases intra-pericardial pressure (cardiac tamponade)
Impaired atrial contraction that can result from atrial arrhythmia such as atrial fibrillation.
Increased heart rate (e.g., atrial tachycardia), which reduces ventricular filling pressure (the pressure that
builds up in the ventricle as the ventricle is being filled with blood).
 Decreased ventricular afterload, which enhances forward flow (i.e., ejection) thereby reducing end-
systolic volume and end-diastolic volume secondarily.
 Ventricular diastolic failure (decreased ventricular compliance) caused, for example, by ventricular
hypertrophy or impaired relaxation (lusitropy).
 Inflow (mitral and tricuspid) valve stenosis, which reduces ventricular filling.
2. Afterload
Afterload is the load on the muscle during contraction (i.e., wall stress during left ventricle ejection)
Afterload is the force that impedes or opposes ventricular contraction.
Afterload is measured clinically by arterial resistance as an estimate of arterial compliance.
Afterload, represent the force that the muscle generates to eject the blood into the aorta.
Afterload is closely related to the aortic pressure. More precisely, afterload is related Left ventricular wall stress:
𝐁𝐥𝐨𝐨𝐝 𝐨𝐫 𝐯𝐞𝐧𝐭𝐫𝐢𝐜𝐮𝐥𝐚𝐫 𝐩𝐫𝐞𝐬𝐬𝐮𝐫𝐞 𝐏 ×𝐋𝐞𝐟𝐭 𝐯𝐞𝐧𝐭𝐫𝐢𝐜𝐮𝐥𝐚𝐫 𝐞𝐧𝐝−𝐝𝐢𝐚𝐬𝐭𝐨𝐥𝐢𝐜 𝐯𝐨𝐥𝐮𝐦𝐞 𝐨𝐫 𝐯𝐞𝐧𝐭𝐫𝐢𝐜𝐮𝐥𝐚𝐫 𝐫𝐚𝐝𝐢𝐮𝐬(𝐫)
Left ventricular wall stress (σ) =
𝐕𝐞𝐧𝐭𝐫𝐢𝐜𝐮𝐥𝐚 𝐰𝐚𝐥𝐥 𝐭𝐡𝐢𝐜𝐤𝐧𝐞𝐬𝐬 𝐡

Blood or ventricular pressure means the pressure inside the ventricle.

The pressure inside the ventricle is actually left ventricular transmural pressure=
Left ventricular pressure (90mmHg) minus intrapleural pressure (10 mmHg) = 80mmHg
According to the to the Law of LaPlace for thin-walled spheres or cylinders, which states that
Wall tension (T) = 𝐏𝐫𝐞𝐬𝐬𝐮𝐫𝐞 𝐏 × 𝐫𝐚𝐝𝐢𝐮𝐬 (𝐫)
𝐖𝐚𝐥𝐥 𝐭𝐞𝐧𝐬𝐢𝐨𝐧 (𝐓)
Then Left ventricular wall stress (σ) =
𝐯𝐞𝐧𝐭𝐫𝐢𝐜𝐮𝐥𝐚𝐫 𝐰𝐚𝐥𝐥 𝐭𝐡𝐢𝐜𝐤𝐧𝐞𝐬𝐬 (𝐡)
The exact equation of Left ventricular wall stress depends on the cardiac chamber shape, which changes during the cardiac cycle; therefore, a single geometric relationship
is sometimes assumed.
For this reason, the above relationship is expressed as a proportionality to highlight how pressure, radius and wall thickness contribute to afterload.
After-load is tension in left ventricular wall that resistance to ventricular ejection; measured clinically as systemic vascular resistance.
)systemic vascular resistance( ‫ ) مقدار الجهد الذي يؤديه جدار البطين حتى يتغلب على مقاومة الشرايين ويحسب ب‬After-load(‫ال‬