Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 686 - файл
.pdf
CHAPTER 8 Respiratory System
201
is characteristic of hypoxaemia due to shunt, and
occurs because of the dierences between the dissociation curves for O2 and CO2.
4. Ventilation and perfusion inequality: (see Ventilation
and Perfusion section), usually seen in chronic lung dis-
ease, i.e. chronic obstructive airways disease (COAD). It
means that ventilation and blood ow are mismatched.
Oxygen therapy can improve the hypoxaemia.
5. Reduction in inspired oxygen tension.
Respiratory Failure
• Respiratory failure is present if PaO2 is <8 kPa; this can
be further divided into types I and II based on the level
of carbon dioxide:
1. Type I: PaCO2 is <6 kPa; it is referred to as hypoxae-
mic respiratory failure. It is due to ventilation–perfusion mismatching. PaCO2 is normal or low as the
increased ventilatory rate in remaining alveoli can
compensate for increases in CO2. Compensation
cannot occur for O2, as the dissociation curve is sigmoid and will reach a plateau:
• causes of type I respiratory failure include:
• pneumothorax
• pneumonia
• contusion
• pulmonary embolism
• ARDS.
2. Type II: PaCO2 is >6 kPa; it is referred to as ventila-
tory failure and is due to inadequate movement of
air. e relative state of hypoventilation causes the
PaO2 to fall and the PaCO2 to rise:
• causes of type II respiratory failure include:
• COPD
• neuromuscular disorders
• airway obstruction
• central respiratory depression
• chest wall deformity.
Clinical Physiology
Response to Hypoxia
Acute
• PaO2 is a relatively weak stimulus to respiration; the
respiratory rate does not alter signicantly until PaO2
falls to 8 kPa.
• e carotid bodies are responsible for detecting this
change and initiating the physiological changes – they
respond to the decrease in PaO2 by increasing the rate
and depth of respiration (minute volume); this leads to
a decrease in PaCO2 and reduced respiratory drive from
the central chemoreceptors.
• In these situations respiration is stimulated by hypoxia
rather than the level of CO2; this is called hypoxic drive.
• e carotid bodies also elicit cardiovascular changes in
response to hypoxia:
• increased heart rate
• increased cardiac output
• vasoconstriction in the skin and splanchnic cir-
culation.
Chronic
ere are several physiological changes that occur with
chronic hypoxia; these include:
• ↑ minute volume: although this causes a respiratory
alkalosis by decreasing PaCO2, there is renal compensation by the excretion of excess bicarbonate.
• ↑ number of red cells and haemoglobin: this is stimulated by erythropoietin, released by the kidney in
response to hypoxia. In addition there is increased
2,3-DPG by red cells; this shis the oxygen dissociation curve to the right and increases the ease of oxygen
release.
• ↑ cardiac output: this produces increased blood ow to
organs and thus increased oxygen delivery.
• ↑ vascularity of organs: the diameter of capillaries
increases and they become more tortuous; this aids in
the delivery of oxygen to the tissues.
Oxygen Therapy and Mechanical Ventilation
Oxygen Therapy
Oxygen therapy can be via variable or xed performance
masks:
• Variable performance masks, i.e. Hudson mask or nasal
cannula, do not deliver a constant concentration of oxygen and are dependent on the patient's peak inspiratory ow rate (PIFR). As PIFR ↑ then more air will be
entrained and will decrease oxygen concentration.
• Fixed performance masks, i.e. Venturi masks, deliver
a constant oxygen concentration, irrelevant of the
patient’s PIFR. e mask entrains air at a xed rate and
thus oxygen dilution does not occur. Dierent colours
signify dierent oxygen ow rates.
Mechanical Ventilation
Indications
ese can be divided into:
• Inadequate ventilation:
• apnoea
• respiratory rate >35
• PaCO2 > 8 kPa.
• Inadequate oxygenation: PaO2 <8 kPa with 60% FiO2.
• Surgical indications:
• head injury
• chest injury
• facial trauma
• high spinal injury.
202
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
SECTION II Physiology
Intermittent positive pressure ventilation (IPPV)
• The basis for mechanical ventilation is called intermittent positive pressure ventilation (IPPV); the
principle of IPPV is the same as normal ventilation
in the fact that air flows down a pressure gradient.
However, during normal ventilation air flows from
atmospheric pressure to negative intra-alveolar pressure; in IPPV the driving pressure is positive to zero
(as opposed to zero to negative). Expiration remains
a passive event.
• Following the decision to commence mechanical ventilation, the settings and mode of ventilation must be
selected.
• An example of initial ventilator settings may be:
• FiO2 = 0.5
• tidal volume = 10–12 mL/kg
• respiratory rate = 10–12 per min
• inspiration:expiration (I:E) ratio = 1 : 2
• limit airway pressure = 40 cmH2O
• positive end expiratory pressure (PEEP) = 2.5–10
cmH2O.
• Modes of ventilation include:
• controlled mandatory ventilation (CMV): the patient
makes no respiratory eort and the ventilator delivers a set volume
• synchronized intermittent mandatory ventilation
(SIMV): the patient requires less sedation and paralysis; the patient receives a combination of ventilator
breaths and breaths initiated by the patient; the ventilator co-ordinates the breaths so that they do not
occur together
• pressure controlled ventilation (PCV): in CMV and
SIMV modes the ventilator will deliver a given volume of air irrelevant of the pressure required to do
so. Controlling the pressure reduces the risk of barotrauma to the lung
• pressure support ventilation (PSV): this mode of ventilation can be used with SIMV and PCV. It allows the
patient to wean from the ventilator by triggering each
breath. e ventilator simply delivers a preset pressure to assist the patient; this pressure can be gradually reduced, allowing the patient to do increasing
amounts of work.
• Another important concept in mechanical ventilation
is the recruitment of collapsed alveoli by using positive
pressure throughout the respiratory cycle. is has the
eect of allowing oxygenation to occur throughout the
respiratory cycle and also increases FRC, which places
the lung on the ecient part of the compliance curve.
Examples of this include:
• PEEP: used during mechanical ventilation
• continuous positive airways pressure (CPAP): used
during spontaneous breathing by a tight-tting facemask
• reversal of I:E ratio: normally the ratio is 1 : 2, which
allows time for passive expiration; increasing the
inspiratory time and allowing less time for expiration
(i.e. 1 : 1, 2 : 1 or 3 : 1) will leave progressively more air
in the alveoli and thus prevent their collapse; this is
called auto-PEEP.
Complications
e complications of mechanical ventilation include:
• ventilator-induced injury
• volutrauma
• barotrauma
• hypotension and decreased cardiac output: decreased
venous return due to positive intrathoracic pressure
• respiratory muscle atrophy
• nosocomial infections
• technical complications, e.g. disconnection
• increase in intracranial pressure (ICP) due to the
increase in intrathoracic pressure.
OSCE SCENARIOS
OSCE Scenario 8.1
A 59-year-old male with severe acute gallstone pancreatitis
has been on the ward for 5 days. He is complaining of acute
shortness of breath with a respiratory rate of 32 and an
SpO2 of 88% despite oxygen by facemask. e junior doc-
tor has obtained arterial blood gases, the results of which
are shown below:
pH 7.25
PaO2 7.7 kPa
PaCO2 7 kPa
Base excess −9 mmol/L
−
HCO
18 mmol/L
3
1. What are the possible dierential diagnoses for the
shortness of breath?
2. How is respiratory failure classied?
3. What is adult respiratory distress syndrome (ARDS)?
4. How is ARDS diagnosed?
5. How is ARDS managed?
CHAPTER 8 Respiratory System
203
OSCE Scenario 8.2
A 52-year-old male, seven days post-right total knee
replacement, has become acutely short of breath. He has
severe chest pain on inspiration.
1. What is the dierential diagnosis?
2. What changes on ECG would support a diagnosis of
He also has pleuritic chest pain. You suspect a pulmonary
embolism (PE).
1. What other signs may be associated with a PE?
2. What would you expect to see on arterial blood gases
and why would you see these changes?
3. How would you investigate and treat this patient?
pulmonary embolism (PE)?
3. What is the treatment for PE?
4. Describe the physiological changes that lead to hypoxia
and hypotension which occur in PE.
OSCE 8.5
A 26-year-old male has been shot in the chest with a shotgun and has a sizeable chest injury. He is very short of
breath. Bubbles are coming from the wound.
OSCE Scenario 8.3
A 19-year-old male is involved in a ght. He has been
stabbed in the le side of the chest. He is brought into A&E
very pale and struggling to breathe.
1. What possible chest injury could he have?
1. What type of chest injury is this and how would you
treat it?
2. He has hypoxia and hypoxaemia – which type of
hypoxia and hypoxaemia does he have?
3. What other types of chest injury can you describe?
2. What would be the examination ndings in each?
3. How would you manage this patient?
OSCE 8.4
Answers in Appendix pages 446–449
A 56-year-old male has recently had major knee surgery
and you are called to the ward as he has diculty breathing.
Please check your eBook at https://studentconsult.inkling.com/ for more self-assessment questions. See inside cover for
registration details.
9
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Cardiovascular System
CARDIAC MUSCLE
• Myocytes surrounded by cell membrane, in which there
are voltage-operated ion channels.
sarcomeres.
• Sarcomeres consist of actin (thin) and myosin (thick)
laments, which are responsible for contraction.
• Actin laments are associated with troponin and tropomysin, which regulate the process of contraction.
• Actin and myosin laments slide over each other to
shorten the sarcomere. Shortening of several sarcomeres
is the mechanism by which the myocyte contracts.
• In the absence of calcium the troponin/tropomysin
complex inhibits cross-bridging between actin and
myosin laments.
• When calcium binds to troponin, formation of crossbridging occurs between the laments. e laments
then slide over one another to cause contraction.
• ATP is required to detach myosin and actin so that the
procedure can be repeated.
• Functionally, heart must act as a syncytium, i.e. a single
cell formed from a number of fused cells. erefore,
when one part of the heart depolarizes, a wave of depolarization passes through the entire cardiac muscle.
• Myocytes contain large numbers of mitochondria, generating energy via aerobic metabolism.
• Myocyte function depends on optimal concentrations
of Ca2+, Na+ and K+.
• Myocytes have two systems of intracellular membranes:
• T-tubules
• sarcoplasmic reticulum.
Cardiac Action Potential (Fig. 9.1)
• e action potential is the electrical signal that travels
throughout the cardiac muscle to initiate contraction.
• Cardiac action potentials have dierent characteristics
in dierent regions of the heart: one for the Purkinje
bres and ventricular muscle, one for atrial muscle and
25 mV
SA node
Atrial muscle
AV node
Bundle of His
Purkinje fibres
Ventricular muscle
100 ms
Fig. 9.1 Shape, duration and sequence of cardiac
action potentials; note also the delays caused by
the anatomical sequence of depolarization and by
the relative conduction velocities down the conducting system. (From Hoffman BF & Cranefield PF.
Electrophysiology of the Heart. McGraw-Hill, New
York, 1960.)
one for the sinoatrial (SA) and atrioventricular (AV)
nodes.
• A typical action potential is divided into four phases:
Phase 0
Initial rapid depolarization, rapid increase in sodium
permeability.
Phase 1
Rapid repolarization, rapid decrease in sodium permeability, small increase in potassium permeability.
204
CHAPTER 9 Cardiovascular System
205
Phase 2
Slow repolarization – plateau eect due to inward movement of calcium. Plateau lasts about 200 ms.
Phase 3
Rapid repolarization – increase in potassium permeability
and inactivation of slow inward Ca2+ channels.
Phase 4
e resting membrane potential of the ventricular muscle
is about −90 mV. e SA node and conducting system do
not have a resting membrane potential – they are constantly depolarizing.
Excitation/Contraction Coupling
• Mechanism by which the cardiac action potential causes
the myobrils to contract.
• Arrival of the action potential allows Ca2+ to move from
the sarcoplasmic reticulum into the cytoplasm.
• Ca2+ binds to troponin C, eventually activating the
actin–myosin complex, resulting in contraction.
• e plateau phase, the result of further calcium inux,
prolongs and enhances contraction.
• e cardiac action potential is very long (200–300 ms).
Aer the contraction there is a refractory period when
no further action potentials can be initiated and therefore no contraction occurs. e long action potential
and refractory periods ensure contraction and relaxation of the heart, allowing the chambers to ll during
relaxation and empty during contraction.
• Intracellular Ca2+ is the most important factor controlling myocardial contractility:
• increased intracellular Ca2+ increases force of myo-
cardial contraction
• decreased intracellular Ca2+ decreases the force of
myocardial contraction.
Generation and Conduction of Cardiac Impulse
• Cardiac tissue has two types of cell:
• cells that initiate and conduct impulses, i.e. SA, AV
nodes
• cells that conduct and contract; muscle mass of the
heart.
• SA node is situated in the right atrium near the entrance
of the superior vena cava (SVC).
• SA node is the pacemaker dictating the rate of beating of
the heart because it has the highest frequency of ring.
• From SA node, action potentials are conducted from
one atrial cell to another, ensuring that both atria contract simultaneously.
• AV node is located in the atrioventricular brous ring
on the right side of the atrial septum. It is the only electrical pathway through the brous ring.
• AV node is activated by atrial electrical activity, which
results in activation of Purkinje cells.
• Conduction through the AV node is slow, delaying
transmission from atria to ventricles, ensuring that
atrial contraction is nished before ventricular contraction begins.
• From the AV node, action potentials travel in the bundle
of His down the ventricular septum and along the right
and le bundle branches to enter the Purkinje system of
bres.
• Conduction is rapid in the Purkinje cells and the action
potential is rapidly transmitted to myocytes at the apex
of the heart.
• Myocytes at the apex of the ventricle are excited and the
action potential spreads upwards towards the brous
ring.
• Cells of the SA node, AV node, Purkinje system have
the ability to depolarize themselves at regular intervals
(self-excitation).
• ese cells also have a long refractory period. erefore
the cells with the highest frequency of ring will control
the heart rate.
• A denervated heart (e.g. transplanted heart) will continue to beat. e rate can increase via circulating
adrenaline but atropine does not have any eect (vagal
denervation) on the heart rate.
• Failure of the SA node results in cells with the next
highest ring frequency, i.e. AV node, taking over pacemaker function.
• Vagal stimulation (parasympathetic) slows the heart by
action on the SA node. Stimulation of the sympathetic
innervation and sympathomimetic hormones act to
increase the heart rate.
Generation of Cardiac Output
• All cardiac muscle has intrinsic capacity for rhythmic
excitation.
• Cardiac tissue spontaneously depolarizes until an action
potential occurs and contraction is initiated. is is
independent of other inuences.
• Various bres have dierent rates of depolarization, but
since they form a functional syncytium with specialized
conducting tissue, depolarization spreads from cell to
cell leading to co-ordinated contraction.
• is rhythmic activity produces alternate contraction/
relaxation, i.e. systole/diastole.
206
Time (s)
R
PP
Right coronary
DiastoleSystoleAS
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
SECTION II Physiology
120
Volume (mL) Pressure (mmHg)Pressure (mmHG)
RIGHT HEART LEFT HEART
Left coronary
blood flow
Zero flow
blood flow
Zero flow
100
120
80
60
40
20
0
80
40
20
10
Right atrium
0
0
0
1st
R
0
2nd
T
Q
S
IRPICP
Ventricle
Atrium
Pulmonary artery
Right ventricle
Heart sounds
0.40.2
Aorta
4th3rd
Q
0.80.6
Fig. 9.2 The cardiac cycle. ICP, Isometric contraction
period, IRP, isometric relaxation period, AS, atrial
systole.
Phases of the Cardiac Cycle (Fig. 9.2)
• Systole:
• contraction (I): mitral and tricuspid valves close
• ejection (IIa, b): aortic and pulmonary valves open.
• Diastole:
• relaxation (III): aortic and pulmonary valves close
• lling (IVa, b, c): mitral and tricuspid valves open.
Phase IVc
• Atrial systole.
• SA node depolarizes.
• Atrial muscle contracts.
• Blood ows through AV valves to ventricles, completing
the last 15% of ventricular lling.
Phase I
• Isovolumetric contraction of ventricles.
• AV valves close.
• Aortic and pulmonary valves close.
• Volume of blood in heart remains constant as pressure
rapidly increases (isovolumetric contraction).
Phase IIa
• Ejection.
• Pressure in ventricles exceeds that in aorta and pulmonary artery; valves open.
• Blood ejected in aorta and pulmonary artery.
Phase IIb
• Ejection.
• Aortic and pulmonary pressures equalize with
ventricles.
Phase III
• Diastolic relaxation.
• Isovolumetric relaxation.
• Ventricular pressure falls.
• Aortic and pulmonary valves close.
Phase IVa
• Filling phase of diastole.
• AV valves reopen.
• Passive ventricular lling.
• Rapid lling of ventricles.
• Low atrial pressures due to ‘suction’ eect results in
rapid lling.
Phase IVb
• Decline in rate of lling as atrial volume increases.
• Finally, active atrial contraction begins again, i.e. phase
IVc.
• During phase III the ventricle ejects about 60% of its
volume, i.e. the ejection fraction.
Ejection fraction
Stroke volume (SV)
=
Left ventricular end
aastolic volume (LVEDV)
di
• During phase IVc the ventricles are topped up by 15% at
rest, but more at higher heart rates.
• Failure of atrial contraction therefore at higher heart
rates, e.g. fast atrial brillation (AF); exercise may be
life-threatening.
CHAPTER 9 Cardiovascular System
120/80
25/15
207
Intracardiac Pressures
Normal values for aortic and intra-cardiac pressures are
shown in Fig. 9.3.
Heart Sounds
First Heart Sound
• Due to closure of AV valves.
• Best heard at apex.
• Louder in mitral stenosis, hyperdynamic circulation,
tachycardia.
Second Heart Sound
• Due to closure of aortic and pulmonary valves.
A
RA
0–4
RV
25
0–4
PA
LA
5–10
LV
120
0–10
• Physiological splitting may occur (A2–P2 intervals).
is is due to prolongation of ventricular ejection periods during inspiration resulting from increased stroke
volume secondary to increased venous return.
Third Heart Sound
• Due to rapid ventricular lling.
• Best heard in children.
Fourth Heart Sound
• Due to ventricular distension (sti ventricle) caused by
forceful atrial contraction.
• Indicates ventricular hypertrophy or heart failure.
Venous Pulse (Fig. 9.4)
a-Wave
• Atrial systole.
• Absent in atrial brillation (AF).
• Cannon waves in complete heart block.
• Giant waves in pulmonary hypertension, tricuspid and
pulmonary stenosis.
c-Wave
• Bulging of tricuspid valve leaets in right atrium during
isovolumetric contraction.
• Synchronous with pulse wave in carotid artery.
v-Wave
• Rise in right atrial pressure before tricuspid valve opens.
x-Descent
• Due to tricuspid valve moving down during ventricular
Fig. 9.3 Normal values for intracardiac, aortic and
systole.
pulmonary artery pressure (mmHg as measured by
cardiac catheterization). A = aorta, PA = pulmonary
artery, RA = right atrium, LA = left atrium, RV = right
ventricle, LV = left ventricle.
a
h
y-Descent
• Tricuspid valve opens.
• Right atrial pressure falls as blood ows to right ventricle.
c
x
v
y
Fig. 9.4 Venous pulses: ‘a’-wave: atrial systole, not seen in atrial fibrillation, increased in tricuspid or pul-
monary stenosis; heart block causes variable ‘a’-waves and even ‘cannon’ waves. ‘c’-wave: leaflets of the
tricuspid valve bulge into the right atrium during isovolumetric contraction. ‘v’-wave: right atrium is rapidly
filled while tricuspid valve is closed. ‘x’-descent: atrium relaxes and tricuspid valve moves down. ‘y’-descent:
tricuspid valve opens, and blood flows from right atrium to right ventricle.
208
CO = stroke volume (SV) heart rate (HR),
×
Stroke volume (energy of contraction)
(initial length of muscle fibre)
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
SECTION II Physiology
Coronary Circulation
See also Chapter 1 – Blood Supply of Heart.
• Coronary blood ow is about 250 mL/min at rest.
• Rises to 1 L/min on exercise.
• Coronary ow is reduced during systole (especially during isovolumetric contraction) due to compression of
the intramyocardial arteries.
• Coronary ow therefore occurs mainly during diastole.
• Conditions resulting in low diastolic BP or increased
intramyocardial tension during diastole (e.g. an
increased end diastolic pressure) may compromise coronary blood ow.
• Subendocardial muscle, where the tension is highest, is
particularly vulnerable.
• Diastolic time is important. At fast rates, inadequate
myocardial perfusion occurs.
• Normally, autoregulation of coronary blood ow occurs
by changes in diameter in the coronary vessels; the
diameter is controlled by vessel tone and wall pressure
exerted by the myocardial muscle.
• e tone of vessels is determined by local metabolites,
adenosine, K+ and lack of oxygen.
Cardiac Output (CO)
• Cardiac output is the volume of blood ejected by the
heart in 1 min.
i.e. 70 mL (SV) 70
(approximately)
• May increase three- to fourfold in strenuous exercise.
• Cardiac index (CI) is the CO per square metre of body
surface area (BSA), i.e. 3.2 L (average).
Regulation of Cardiac Output
Regulation of the vascular system ensures that:
• Each organ receives its minimum required blood ow.
• Redistribution of blood ow occurs where appropriate.
• e heart is not overtaxed by providing maximal blood
ow to organs that do not require it.
• e heart has the capacity to increase or decrease its
output according to demand.
• Each organ has its own mechanism for achieving adequate blood ow.
Starling’s Law of the Heart (Fig. 9.5)
• Starling’s law: the energy of contraction of a cardiac
muscle bre is a function of the initial length of the
muscle bre.
• e greater the stretch of the ventricle in diastole, the
greater the stroke volume.
× bpm (HR) = 5 L/min
Sympathetic
stimulation
Normal
Failing
heart
End diastolic volume
Fig. 9.5 Starling’s law of the heart. In humans the
initial fibre length cannot be measured, so end diastolic volume is used instead.
• e more blood in the heart, i.e. the higher the enddiastolic volume, the more sarcomeres are stretched.
• Up to a point, increasing the venous return increases the
force that the heart muscle can exert.
• Beyond the critical point, further increase in the amount
of blood decreases the force that the heart muscle can
exert.
Factors Modifying Cardiac Output
• Heart rate:
• intrinsic rhythmicity
• extrinsic factors:
• sympathetic increases rate and force
• parasympathetic reduces rate.
• Stroke volume:
• contractility
• preload
• aerload.
1 Contractility
• e force of myocardial contraction determines the CO,
SV and myocardial O2 demand.
• Causes of increased contractility include:
• increased preload
• sympathetic nerve stimulation
• increased extracellular calcium
• drugs: inotropes, digoxin
• hormones: catecholamines, thyroxine, glucagons.
• Causes of decreased contractility:
• reduced lling (Starling’s law)
• hypoxia
• hypercapnia
• acidosis
• ischaemia and cardiac disease
• parasympathetic stimulation
CHAPTER 9 Cardiovascular System
209
• electrolyte imbalance: Ca2+, K
+
• drugs: beta-blockers, antiarrhythmic drugs,
anaesthetics.
• Contractility measured by:
• stroke volume and CO
• ejection fraction on echocardiography.
2 Preload
• Dependent on:
• venous return
• atrial systole (brillation)
• myocardial distensibility.
• Measured by:
• central venous pressure (CVP)
• pulmonary artery occlusion pressure (PAOP).
3 Afterload
Aerload is the tension in the ventricular wall during ventricular ejection.
• Increased by:
• raised aortic pressure
• aortic valve resistance (aortic stenosis)
• ventricular cavity size; increased ventricular volume;
requires greater tension to contract (Laplace’s law)
• raised systemic vascular resistance (SVR), e.g. shock
• increased aerload increases cardiac work and therefore oxygen consumption.
• Decreased by:
• vasodilator drugs: at constant preload and contractility, SV is inversely related to aerload, i.e.
decrease in the peripheral resistance with a vasodilator increases SV
• vasodilator metabolites in septic shock.
Measurement of Cardiac Output
Cardiac output may be measured by the following methods:
• Fick method.
• ermodilution.
• Dye dilution.
• Doppler ultrasound.
e direct Fick method is rarely used in clinical prac-
tice, but most methods are based on this principle. e
thermodilution method and Doppler ultrasound are more
likely to be used in clinical practice.
Fick Method
• Fick principle states that the amount of substance taken
up by an organ per unit time is equal to the blood ow
multiplied by the dierence in concentration of that
substance between arterial and mixed venous blood.
• O2 consumption by whole body is measured for about
15 min. During this time, blood samples are taken from
a systemic artery and pulmonary artery (mixed venous)
blood:
Oxygen consumption rate by body (mL/min)
CO =
i.e.
Arterial O
190 mL O/L blood 140
2mmixed venous O
2
250 mL O/min
2
2 mmL O /L blood
2
2
2
CO = 5 L/min
Thermodilution
is is the most commonly used technique in the intensive
treatment unit (ITU).
• A bolus of ice-cold 5% dextrose is rapidly injected into
the right atrium via the proximal lumen of a pulmonary
artery catheter.
• e dextrose mixes with blood and causes a fall in temperature, which is recorded by a thermistor at the catheter tip in the distal pulmonary artery.
• Computerized integration of the temperature curves
allows derivation of the CO.
• When CO is known it is possible to calculate SVR,
pulmonary vascular resistance (PVR) and ventricular
stroke work.
Dye Dilution
• Uses the same principle as the thermodilution technique but a dye is used rather than ice-cold dextrose.
Doppler Ultrasound
• A Doppler probe is placed in the suprasternal notch.
• Changing frequency of ultrasound waves caused by
reection from blood moving through the ascending
aorta is detected.
• From analysis of the velocity waveform and aortic diameter, the stroke volume can be estimated and hence CO
measured.
Blood Pressure
• BP = CO × SVR.
• Systolic pressure = maximum pressure recorded during
systole (100–200 mmHg).
• Diastolic pressure = minimum pressure recorded during diastole (60–80 mmHg).
• Pulse pressure = systolic pressure minus diastolic pressure (40 mmHg).
• Mean arterial pressure = diastolic pressure plus ⅓ of the
pulse pressure (70 mmHg).
210
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
SECTION II Physiology
Control of Blood Pressure (General
Systemic Blood Pressure)
• Regulation of CO and SVR controls BP.
• Baroceptors of the autonomic nervous system (aortic
arch and carotid) and higher centres of midbrain exert
eects on BP.
• Baroceptors are stretched by increased BP; this leads to
reex reduction in vasoconstriction and venoconstriction, and reduction in heart rate, with consequent fall in
SVR, CO and BP.
• When BP falls baroceptors are less stretched; vasoconstriction, venoconstriction and heart rate increase and
BP rises in reex.
• Autonomic neuropathy may render these reexes
ineective.
• Renin–angiotensin mechanism also controls BP.
Factors Determining Arterial Blood Pressure
• Systolic pressure increases when there is an increase in:
• stroke volume
• ejection velocity (without an increase in stroke volume)
• diastolic pressure of the preceding pulse
• arterial rigidity (arteriosclerosis).
• Diastolic pressure increases when there is an increase in:
• total peripheral resistance
• arterial compliance (distensibility)
• heart rate.
Control of Local Blood Pressure and Blood Flow
e overall determinant of ow is CO, but each organ has
its own superimposed regulatory mechanisms. Regulation
of blood ow is mainly achieved by alteration to the diameter of vessels, which is inuenced by the smooth muscle of
the vessel walls.
Tone in smooth muscle is aected by:
• neural activity, e.g. sympathetic, parasympathetic
• hormones, e.g. adrenaline, noradrenaline, vasopressin,
angiotensin
• local control – autoregulation: hypoxia, adenosine,
nitric oxide, CO2, H+, K+, prostaglandins.
Peripheral Resistance (Systemic Vascular
Resistance; SVR)
• Resistance to ow of blood through arterioles.
• By constricting and dilating, arterioles control the blood
ow to capillaries according to local needs.
Mean arterial pressure
mean right atrial pressure
SVR =
2
rrdiac output
Ca
• Repeated measurements of SVR in the critically ill
patient are useful in monitoring the eects of uid and
inotropic therapy.
Monitoring the Circulation
• ere is no one single monitoring measure which will
dene the problem.
• A series of measurements and monitoring systems over
a period of time is required.
Methods used include:
• ECG
• blood pressure
• central venous pressure
• pulmonary wedge pressure (pulmonary artery occlusion pressure)
• pulse oximetry
• cardiac output
• urine output
• echocardiography
• echo Doppler.
ECG
e events recorded in a standard ECG recording are
shown in Fig. 9.6. e ECG gives information on:
• heart rate
• rhythm (regular or irregular)
• disorders of conduction or excitation
• size and muscle mass of the heart
• damage, e.g. ischaemia or infarction, to dierent parts
of the heart
• electrolyte disturbances, e.g. K+, Ca
• pericardium, e.g. inammation or eusion.
Blood Pressure
• Monitored by manual sphygmomanometry, automatic
dynamap, or best by intra-arterial catheter, usually in
the radial artery.
• In the critically ill there should be continuous observation of the pressure trace.
• e rate of pressure increase (up-slope) of the pressure
trace is proportional to myocardial contractility.
• e area under the wave-form is proportional to stroke
volume.
Central Venous Pressure
• Gives a good indication of preload in patients with
normal heart.
• Useful guide to uid replacement in hypovolaemic
patients, e.g. dehydration, haemorrhage.
• Cannula inserted via internal jugular vein; tip should be
in right atrium.
2+
Соседние файлы в папке @xirurgi_2025