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Chemical and Physical Restraint of Wild Animals
2.3.2 The heart
Cardiac cycle
The heart is a muscular pump that propels
Left
blood through the blood vessels by alternately
atrium
relaxing and contracting. As the heart relaxes,
Right atrium
blood returning via the veins flows into the atria
Left
and directly into the ventricles below. During
ventricle
Right ventricle
contraction, the atria initially start contracting
which forces more blood into the ventricles.
ATRIAL CONTRACTION
MID-DIASTOLE
The atria ‘supercharge’ the ventricles. Ventricular
contraction forces blood out of the left ventricle
into the aorta and out of the right ventricle into
the pulmonary artery. The heart then relaxes and
the cycle starts again. The period during which
the ventricles are contracting and ejecting blood
into the aorta and pulmonary artery is termed
ISOMETRIC
ventricular systole. This is followed by ventricular
VENTRICULAR
diastole during which the ventricles relax and refill
RELAXATION
Figure 2.14: The cardiac cycle
with blood before contracting again (Figure 2.14).
The direction of blood flow from the atria to the
ventricles and then from the ventricles into the
arterial system is controlled by valves, which are
Mitral valve
illustrated in Figures 2.13 and 2.15. As the ventricles
Cusp
begin to contract during systole, the pressure in the
Chordae tendineae
ventricle increases, forcing blood to start flowing
Papillary muscles
back into the atria, which causes the atrioventricular
valves (valves between the atria and ventricles)
to snap closed. The sound caused by the valves
closing is the first sound heard when listening to
the heart with a stethoscope (Lup). As the pressure
Cusp
continues to increase in the ventricles, the aortic
Aortic valve
and pulmonic (tricuspid/bicuspid) valves are forced
open and blood is ejected into the arterial tree. At
the end of systole, the heart relaxes into diastole
and a backflow of blood from the arteries into the
Figure 2.15: Mitral and aortic valves
left and right ventricles causes the tricuspid and
bicuspid valves to snap closed producing the second heart sound (Dup). The heart sounds are not caused by
the movement of the valves themselves but rather the sudden stopping of the backflow of blood as the valves
close. This creates a vibration in the blood and cardiac walls, which are the sounds heard. Ventricular systole is
sometimes defined as that part of the cardiac cycle between the first and second heart sounds.
The contraction of the heart is initiated by groups of specialized cardiac muscle cells called pacemaker cells.
These cells have the ability to depolarize spontaneously, establishing an electrical signal or action potential
that causes the cells of the cardiac muscle to start contracting. This means that the heart does not need to be
stimulated by nerves in order to contract, the nerve supply to the heart rather assists in controlling the rate
and force of cardiac contraction. A group of pacemaker cells termed the sinoatrial (SA) node located in the right
BASIC PHYSIOLOGY
Electrical activity
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Chemical and Physical Restraint of Wild Animals
atrial wall (Figure 2.16) is responsible for initiating
the contraction of the heart. The action potential
this node creates propagates from one cell to the
next of the atria, causing them to contract one after
Vagi
the other. This wave of depolarization passes from
the atria to the ventricles via the atrioventricular
(AV) node. The action potential then travels
rapidly to the rest of the ventricles via a network
Sympathetic
of specialized cardiac cells called the Purkinje
nerves
fibres, resulting in a coordinated and synchronous
Sympathetic
nerves
contraction of the ventricles. The passage of the
action potential through the heart causes the atria
to contract almost simultaneously. This is followed
by a brief pause as the action potential passes
through the AV node and then the two ventricles
contract almost simultaneously. Finally, the entire
Figure 2.16: Autonomic nerve supply to the heart
heart relaxes and refills.
The contraction of the atria and ventricles is
due to an action potential, which passes from one
muscle cell to the next causing them to contract
in sequence. Unlike skeletal muscles, the action
potential in cardiac muscle is able to jump from
cell to cell, causing it to act as if it were a single cell.
Internodal
pathways
Due to this capability, the heart is often referred to
as a functional syncytium (Figure 2.17).
Sinus node
The SA-node discharges at a rate of
approximately 72 cycles per minute in humans;
A-V node
the AV-node has a rate of discharge of its own
A-V bundle
that is much slower – approximately 45 cycles per
Left bundle
minute – but is stimulated to discharge by each
branch
impulse from the SA-node that reaches it. The rate
Right bundle
at which the SA-node depolarizes determines the
branch
heart rate. Both the heart rate and the strength
of myocardial contraction are controlled by
the autonomic nervous system through nerve
endings at the SA-node and myocardium. The
sympathetic nervous system stimulates the SAFigure 2.17: Purkinje system
node to increase heart rate (Figure 2.16). The
parasympathetic nervous system, in the form of nerve endings of the vagal nerve, slows the heart by
inhibiting the SA-node. Adrenaline and noradrenaline released from the adrenal glands and circulating in
the bloodstream have the same effects on the heart as sympathetic nervous system activity. Due to the
interaction between the sympathetic and parasympathetic systems, the heart rate can be adjusted over a
wide range. The highest rates occur during exercise or the fight or flight response when sympathetic activity
predominates and parasympathetic activity is reduced. In a resting or sleeping animal, the sympathetic
system is less active and parasympathetic action prevails to decrease the heart rate. As well as increasing heart
rate by acting on the SA-node, sympathetic nerves also innervate all cardiac cells and increased stimulation
makes each cardiac contraction stronger, quicker and shorter. The activity of the parasympathetic system by
comparison is largely limited to depressing the rate of discharge of the SA- and AV-nodes.
Sympathetic chains
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Chemical and Physical Restraint of Wild Animals
Cardiac output
The volume of blood pumped per cycle or beat of the heart is called the stroke volume. The number of
heartbeats per minute is called the heart rate. Cardiac output is the total volume of blood pumped by the
heart per minute and equals stoke volume multiplied by heart rate.
The total blood volume of an animal is circulated each minute. The
blood volume can be estimated at 8% of body mass. The mass of a
male lion = 200 kg, blood volume = 16 ℓ, at a heart rate of 50 beats/
minute and the stroke volume = 320 ml. An elephant bull has a body
mass of approximately 6 000 kg, blood volume = 480 ℓ, heart rate is
perhaps 40 beats/minute and stroke volume = 12 ℓ.
BASIC PHYSIOLOGY
An increase in cardiac output can thus only be achieved by increasing either the stroke volume, heart rate
or both. The volume of venous blood that returns to the heart is an important factor in determining stroke
volume. The greater the volume of venous return, the greater the stretch it produces in the myocardium.
The stretching of the myocardium increases the force of its contraction and thus the stroke volume – this
is ‘Starling’s law of the heart’. As a general rule, the cardiac output increases to deal with the total volume of
blood returning to the heart. Once the stroke volume reaches a maximum capacity, the heart rate increases
to meet this extra need.
The rate at which the heart contracts per minute is the product of the time taken for the process of
muscular contraction to take place and the period of relaxation that follows. Filling of the ventricles takes
place during diastole and the duration of diastole is determined by heart rate. As heart rate increases, the
length of diastole and the time for ventricular filling decreases. The duration of systole by comparison
remains relatively constant. Complete ventricular filling can take place until the heart rate increases to greater
than about 160 beats per minute. At the higher rates, the amount of ventricular filling starts to decrease,
which would dramatically reduce stroke volume if not for a compensatory mechanism brought about by
the sympathetic nervous system. As has been explained earlier, sympathetic stimulation of the heart not
only increases the rate of contraction but also results in stronger, quicker and shorter contractions of the
ventricles. This means the ventricles empty more completely during each contraction, which helps maintain
stroke volume. It also shortens the duration of systole, which helps preserve diastolic filling time. Table 2.1
summarises the proportion of time taken by diastole and systole as the heart rate increases in humans.
A number of factors will influence the volume of blood returning to the heart, the degree of ventricular
filling and therefore cardiac output. These include increased activity of an animal. Contraction of skeletal
muscles causes the body of the muscles to expand, compressing the veins that run alongside them. This
squeezes the vessels, forcing blood flow towards the heart. Veins have valves spread throughout their length
that prevent blood flowing back towards the tissues (Figure 2.13). As an animal inhales, pressure decreases
in the thorax and increases in the abdomen. This allows the veins in the chest to expand, which draws blood
forward. At the same time, blood is pushed
out of the abdomen due to the increased
Time in seconds
pressure that compresses the veins in this area
Heart rate
Cardiac cycle
Diastole
Systole
of the body. Decreases in total blood volume
due to blood loss (haemorrhage), decrease in
72/min
0,83
0,5
0,33
the amount of water in the extracellular fluid
216/min
0,28
0,06
0,22
(dehydration), or a decrease in the number
Table 2.1: Diastolic and systolic time periods in relation to the time
of red blood cells in the blood (anaemia) will
taken for the complete cardiac cycle
reduce the filling of the heart.
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Chemical and Physical Restraint of Wild Animals
• The amount of haemoglobin in the blood, which determines how much oxygen and carbon dioxide
can be carried. The majority of O2 and, to a lesser degree, CO2 are transported by haemoglobin in the red
blood cells. Any decreases in the concentration of haemoglobin, for example in the case of anaemia, will
reduce the amounts of both gases transported by the blood.
• The thickness of the membranes through which the gases diffuse. Oxygen moves through the airblood barrier, which is made up of the membranes of the alveolus and perfusing capillary (Figure 2.24). Any
increase in thickness of this barrier in cases of disease will increase the time taken for diffusion and reduce
the volume of O2 moving from alveolus to capillary. Carbon dioxide is rarely affected by lung disease as it
has a much higher solubility than O2.
2.4.4 The transport of oxygen and carbon dioxide in the blood
• The partial pressure of oxygen in the air that is breathed. The proportion of O2 to N2 in the air does
not change significantly as altitude increases, but the atmospheric pressure decreases. The decrease in
atmospheric pressure results in a lowering of the partial pressures of both gases. The partial pressure of O2
is the driving force that determines the saturation of haemoglobin. Therefore, animals at higher altitudes
are breathing ‘less’ O2.
BASIC PHYSIOLOGY
The two gases are transported in different ways in the blood. As O2 is poorly soluble in water, only a small
amount dissolves in the plasma of the blood. Most O2 is transported attached to haemoglobin, a pigment
found in red blood cells. Each haemoglobin molecule is able to bind up to four molecules of O2. The
structure of the haemoglobin determines how this occurs. Iron atoms held within the haemoglobin form
the site where oxygen attaches. The attachment is termed oxygenation. When the oxygenated haemoglobin
reaches the tissues, oxygen is released from the
molecule and moves out of the circulation into
the tissues. The driving force for the movement
of oxygen is the partial pressure of the gas –
relatively high in the alveolar air and low in the
tissues where it is utilised (Figure 2.25). A small,
and insignificant, proportion of the total oxygen
content of blood is dissolved in plasma. Once
again, this amount is the product of the partial
pressure of the gas.
Haemoglobin’s affinity for oxygen is influenced
by several factors: the most important being
the partial pressure of O2 in the alveolar air
and also in blood. This means that the degree
of saturation of haemoglobin by O2 increases
or decreases together with the partial pressure
of the gas. Haemoglobin is 100% saturated
at a partial pressure of 100 mmHg, which is
the approximate partial pressure of the gas in
alveolar air. As oxygenated blood passes through
the tissues, where the partial pressure of O2 may
vary between 5 and 40 mmHg, O2 is released. At
Figure 2.25: The carriage of oxygen by haemoglobin and the
a partial pressure of 40 mmHg, haemoglobin is
oxygen – haemoglobin dissociation curve
70% saturated, as it has released 30% of the O2
it carries.
The amount of oxygen made available to the tissues is influenced by:
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Chemical and Physical Restraint of Wild Animals
• The concentration of haemoglobin in the blood. A gram of haemoglobin can carry 1,34 ml of O2. The
standard or expected concentration of haemoglobin in the blood will be in the region of 150 g/ℓ and thus
1 litre of blood will carry 150 x 1,34 ml = 200 ml of O2. An average of 50 ml/ℓ of O2 will be utilised by the
tissues at rest. Certain species, such as the horse, are able to increase the number of red blood cells and
therefore the haemoglobin circulating in the blood, by contracting their spleen during exercise. This forces
stored red blood cells into circulation.
• The affinity of haemoglobin for oxygen. The amount of O2 that binds to haemoglobin is influenced by a
number of factors, including temperature, pH and partial pressure of CO2. An increase in the temperature of
a tissue due to increased metabolism, causes haemoglobin to release the O2 that it is carrying in those areas
where it is required most. An increase in metabolism also results in higher concentrations of CO2 and hydrogen
ions with a decrease in pH. Haemoglobin releases larger amounts of O2 as a consequence of these changes.
The presence of 2.3-diphosphoglycerate in red blood cells facilitates the binding of O2 with haemoglobin.
• The volume of blood flowing through the tissues. The delivery of more O2 to tissue with increased
metabolic rates starts with increasing the supply of oxygenated blood to these areas.
Haemoglobin saturated with oxygen causes blood
to be a cherry red colour; as the blood becomes
desaturated, it darkens, becoming almost black in
extreme cases.
Carbon dioxide is transported in several forms
(Figure 2.26):
•approximately 7% is dissolved in plasma and
transported in solution
•70% enters the red blood cells where it binds
with water to form hydrogen and bicarbonate
ions (the later moving out of the red blood cells
into the plasma)
Figure 2.26: The carriage of CO2 in the blood
• 23% combines with haemoglobin.
During strenuous exercise, the demand for O2 due to increased cell metabolism in tissues, especially muscles,
can rise by 30-fold. This extra demand for O2 is met by various strategies. Cardiac output increases, causing
more blood to flow through the lungs per minute, allowing for a greater rate of gaseous exchange. It also
increases the volume of blood supplied to the exercising muscles. Certain species including horses are able
to increase the number of circulating red blood cells and therefore the amount of haemoglobin available to
bind with and transport O2. Exercising muscles are able to extract more O2 from blood than those at rest. This
is due to the greater diffusion gradient for O2 created by the increased consumption of O2 by the muscles. An
increase in temperature and lowering of pH at the muscles reduces the affinity of haemoglobin for O2.
2.4.5 Regulation of respiration
Respiration is controlled in the medulla of the brain (CNS), and is modified by higher brain centres and inputs
from peripheral receptors to regulate tidal volume and respiratory frequency. Three groups of neurons located
within the pons and medulla of the brain stem are involved in the control of respiration. They adjust the rate
and depth of respiration as the need arises. The central chemoreceptor, a chemosensitive region located within
these neurons responds to changes in the level of CO2 in the blood, which is the primary moderating stimulus
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Chemical and Physical Restraint of Wild Animals
Medulla
Glossopharyngeal
nerve
Chemosensitive
area
Inspiratory
area
Vagus nerve
Carotid body
H+ + HCO3H2CO3
Aortic bodies
CO2 + H2O
Figure 2.27: The regulation of respiration by the
respiratory centre in the medulla oblongata
Figure 2.28: The chemoreceptors that measure PO2
levels in arterial blood
of respiratory rate and depth (Figure 2.27). The CO2 from the blood crosses the blood-brain barrier and enters
the cerebrospinal fluid (CSF), which bathes the central chemoreceptor. It binds with water to form carbonic
acid, which dissociates into bicarbonate (HCO2-) and hydrogen (H+) ions. An increase in CO2 in the blood
causes an increase in the H+ in the CSF, which stimulates ventilation. The opposite happens with decreasing
levels of blood CO2. Hydrogen ions produced by metabolism will have a similar stimulating effect upon
respiration. Peripheral chemoreceptors located in the carotid and aortic bodies (Figure 2.28) monitor levels of
O2 in the blood. However, under normal circumstances they do not affect respiration due to the dominant
influence of CO2 on the central chemoreceptor. It is only at low levels of O2, e.g. below 60 mmHg in humans,
that the peripheral chemoreceptors start influencing respiration and stimulate ventilation. Pulmonary stretch
receptors located in the smooth muscle of the trachea and bronchi are believed to assist in regulating
respiration. As the lungs expand during inspiration, these receptors become more active until they inhibit
breathing, allowing the lungs to relax and resulting in expiration. Stretch receptors located in the intercostal
muscles, and to a lesser extent the diaphragm, control the strength of contraction of these muscles.
!
2.4.6 The importance of respiratory physiology in the immobilization of wildlife
1. Opioids, including morphine derivatives such as etorphine, suppress the response of the respiratory
centres to CO2. The reduction of alveolar ventilation results in hypoxia and hypercapnea.
2. When a herbivore goes down into lateral or sternal recumbency, these changes in posture result in the
gut contents, rumen or massive large colon pushing forward onto the diaphragm and preventing it from
moving backward when it contracts. Alveolar ventilation is reduced due to a reduction in lung volumes.
3. Changes in posture change the dynamics of blood flow and ventilation in the lungs. Areas in the lungs
may be well ventilated but less well perfused by blood, or blood flow is increased in areas of lung where
ventilation is reduced. This is called a ventilation/perfusion mismatch and results once again in hypoxia
and hypercapnea.
It is important that we are aware of these effects and monitor the animal’s responses to ensure that it is
able to cope with the changes. Failure to do so may result in death.
BASIC PHYSIOLOGY
4. The elephant is the only animal in which the lungs are attached to the thoracic wall. In addition, the
relative lung size of the elephant is small. Although these animals respond well to immobilization with
opioids, they should generally not be left in sternal recumbency for more than 15 minutes.
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