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understanding pathophysiology

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understanding
pathophysiology

Judy Craft
Christopher Gordon
Adriana Tiziani
Sue E Huether
Kathryn L McCance
Valentina L Brashers
Neal S Rote
 23
ALTERATIONS OF
CARDIOVASCULAR FUNCTION
ACROSS THE LIFE SPAN
KEY TE R MS
acute coronary syndromes,
628
acute myocardial infarction
(AMI), 628
acute onset of systolic left
heart failure, 669
anaphylactic shock, 678
C HAP TE R OUTLINE angiotensin-converting
enzyme (ACE) inhibitors, 612
aneurysm, 637
Introduction, 607 angina pectoris, 625
Alterations of blood flow and pressure, 607 aortic regurgitation, 654
Hypertension, 607 aortic stenosis, 647
Orthostatic hypotension, 614 arrhythmias, 661
Arteriosclerosis, 617 arteriosclerosis, 617
Atherosclerosis, 617 atherosclerosis, 617
Coronary heart disease, 621 atrial septal defect (ASD), 644
Myocardial ischaemia, 624 atrioventricular canal (AVC)
The acute coronary syndromes, 628 defect, 645
Aneurysm, 637 cardiogenic shock, 678
Thrombus formation, 638 cardiomyopathies, 651
Embolism, 638 chronic left heart failure, 672
Peripheral artery disease, 639 coarctation of the aorta, 647
Alterations to veins, 639 congenital heart disease, 642
Alterations of cardiac function, 642 congestive heart failure, 675
Congenital heart disease, 642 coronary angiography, 626
Defects with increased pulmonary blood flow, 644 coronary artery bypass graft,
Defects with decreased pulmonary blood flow, 646 627
Obstructive defects, 647 coronary heart disease, 621
Mixing defects, 648 cyanosis, 642
Acquired cardiovascular disorders, 649 diastolic heart failure, 672
Alterations of the heart wall, 650 dyslipidaemia, 621
Disorders of the pericardium, 650 embolism, 638
Disorders of the myocardium: the cardiomyopathies, 651 embolus, 638
Disorders of the endocardium, 652 hibernating myocardium, 633
Alterations of cardiac conduction, 661 high-density lipoproteins
Arrhythmias, 661 (HDL), 621
Heart failure, 666 hypertension, 607
Left heart failure, 666 hypovolaemic shock, 678
Right heart failure, 672 infective endocarditis, 659
Heart failure in children, 675 Kawasaki disease, 649
Shock, 675 left heart failure, 666
Impairment of cellular metabolism, 676 low-density lipoproteins
Types of shock, 678 (LDL), 621
Multiple organ dysfunction syndrome, 682
606
Craft_004.indb 606
mitral regurgitation, 656
mitral stenosis, 654
mitral valve prolapse
syndrome, 657
multiple organ dysfunction
syndrome (MODS), 676
myocardial ischaemia, 624
myocardial remodelling, 633
myocardial stunning, 633
neurogenic shock, 678
non-ST elevation MI (non-
STEMI), 629
patent ductus arteriosus, 645
percutaneous transluminal
coronary angioplasty
(PTCA), 627
pericardial effusion, 651
peripheral artery disease, 639
Prinzmetal’s angina, 625
pulmonary stenosis, 648
rheumatic heart disease, 657
right heart failure, 672
septic shock, 680
shock, 675
silent ischaemia, 625
ST elevation MI (STEMI), 629
stable angina, 625
superior vena cava
syndrome, 641
systemic inflammatory
response syndrome (SIRS),
680
systolic heart failure, 666
tetralogy of Fallot, 646
transposition of the great
arteries (TGA), 648
tricuspid regurgitation, 656
truncus arteriosus, 649
unstable angina, 628
valvular regurgitation, 652
valvular stenosis, 652
varicose vein, 640
venous thromboembolus, 639
ventricular septal defect
(VSD), 644
31/08/10 2:39 PM
 chapter 23 • alterations of cardiovascular function across the life span
INTRODUCTION
Cardiovascular diseases are conditions and diseases
that affect the heart and vasculature (blood vessels).
There are variations in the definition of cardiovascular
diseases, with some classifications including heart
disease, vascular disease, stroke and circulatory disease.
The most common forms of cardiovascular diseases are
hypertension, coronary heart disease, heart failure and
cerebrovascular disease. Cerebrovascular disease arises
from pathological processes in blood vessels of the brain,
with stroke being the most frequent manifestation of
cerebrovascular disease. Although stroke is classified as
a cardiovascular disease, it is discussed in Chapter 9 to
consider the effects on the brain.
In Western countries, cardiovascular disease is an
epidemic and major health problem. Approximately 18%
of Australians (3.5 million people) are reported to have a
long-term cardiovascular condition, with the prevalence
of disease increasing with age (see Figure 23-1).
In addition, cardiovascular disease remains a major
contributor to mortality, accounting for 36% and 40%
of all deaths in Australia and New Zealand, respectively.
In more recent years, there has been a reduction in the
mortality rate attributable to cardiovascular disease due
to improvements in cardiovascular disease management
and a lowering of some risk factors (such as smoking).1
Unfortunately, these reductions are somewhat offset by
the increased prevalence of cardiovascular disease in the
elderly, combined with increasing rates of obesity and
diabetes mellitus in the population (see Chapter 35). In
addition, most people are afflicted with more than one
cardiovascular condition and many have multiple cardio-
vascular risk factors. Furthermore, in both Australia and
New Zealand cardiovascular disease is more prevalent in
the Indigenous population than in the non-Indigenous
population.2,3
80
Males with cardiovascular disease
Prevalence (%)
60
Females with cardiovascular disease
40
20
0 blood pressure (BP) measurements at different times,
0–14 15–24 25–34 35–44 45–54 55–64 65–74 75 and
over
Age group (years)
FIGURE 23-1 Reported prevalence of cardiovascular conditions
in Australia across age groups.
Source: Australian Bureau of Statistics. National Health Survey
Australia, 2004–05. Canberra: ABS. Note: 2007–08 data unavailable at
time of writing.
Craft_004.indb 607
607
It is vital that you have a comprehensive understanding
of the pathophysiology of cardiovascular conditions, due
to the high prevalence of cardiovascular disease in the
community. Nurses are more actively involved than
they have been previously in the management of cardio-
vascular conditions such as hypertension and heart
failure, and your comprehension of the pathophysiology
will aid your ability to care for individuals with
cardiovascular conditions.
ALTERATIONS OF BLOOD FLOW AND
PRESSURE
Pathophysiological alterations to arteries and veins
include hypertension, atherosclerosis and peripheral
vascular disease, and all of these conditions can lead
to other cardiovascular diseases. The damage to the
arteries in particular can lead to coronary heart disease,
cerebrovascular disease or heart failure — the top three
causes of death due to cardiovascular disease in Australia
and New Zealand.1 This section details the formation
of arterial and venous alterations, which will aid your
understanding of the primary cardiovascular diseases.
We start with the most common cardiovascular condition
worldwide, hypertension.
Hypertension
Hypertension, or high blood pressure, is consistent
elevation of systemic arterial blood pressure. It con-
siderably increases the individual’s risk of developing
coronary heart disease, heart failure and strokes. It
is the most prevalent cardiovascular condition and is
estimated to afflict about one billion people worldwide
— just over one-quarter of the world’s adult population.4
Approximately 3.7 million Australians over the age
of 25 years (30% of adults) have high blood pressure
or are on medication to treat high blood pressure.1
Unfortunately, evidence suggests that a large number of
adults and children have undiagnosed hypertension.5,6
The prevalence of hypertension increases in the elderly
and in Aboriginal and Torres Strait Islander peoples and
Maori and Pacific Islander peoples compared to the non-
Indigenous population.1,3
The diagnosis of hypertension is based on repeated
when systolic blood pressure is equal to or greater than
140 mmHg or diastolic pressure is 90 mmHg or greater
(see Table 23-1).7 Normal blood pressure is associated
with the lowest cardiovascular risk, whereas those who
fall in the ‘high–normal’ range are at risk for developing
hypertension unless they institute lifestyle modifications
(in fact, more than 90% will develop hypertension8).
31/08/10 2:39 PM
 610 PART FOUR alterations to body maintenance
dietary intake of potassium, magnesium and calcium;
and obesity.12 Dysfunction of these hormones, along
with alterations in the renin-angiotensin-aldosterone
system and the sympathetic nervous system, cause an
increase in vascular tone and a change in the pressure–
natriuresis relationship. Sodium retention leads to water
retention, causing an increase in blood volume, which
contributes to elevations in blood pressure. Subtle renal
injury results, with renal vasoconstriction and tissue
ischaemia. Tissue ischaemia causes inflammation of the
kidneys, and contributes to dysfunction of the internal
structure of the kidneys, namely the glomeruli and
tubules, which actually promotes additional sodium
retention. This vicious cycle leads to increases in blood
pressure at rest and eventually hypertension.
Inflammation plays a role in the pathogenesis of
hypertension. Endothelial injury and tissue ischaemia
result in the release of vasoactive inflammatory cytokines
(see Chapter 13). Although many of these cytokines
(for instance, histamine) have vasodilatory actions
in acute inflammatory injury, chronic inflammation
contributes to vascular remodelling and smooth muscle
contraction. Endothelial injury and dysfunction in
primary hypertension are further characterised by a
Genetic influences
Defects in
Functional,
renal sodium
vasoconstriction
haemostasis
Inadequate sodium
excretion
CONCEPT MAP
Sodium and water
retention
Natriuretic
hormone
Plasma and ECF Vascular
volume reactivity
Cardiac output
(autoregulation)
Hypertension
FIGURE 23-4 The pathophysiology of primary hypertension.
A hypothetical scheme for the pathogenesis of essential hypertension, implicating genetic defects in renal excretion of sodium,
functional regulation of vascular tone and structural regulation of vascular calibre. Environmental factors, especially increased sodium
intake, may potentiate the effects of genetic factors. The resultant increases in cardiac output and peripheral resistance contribute to
hypertension. ECF = extracellular fluid.
Source: Modified from Kumar V. Robbins & Cotran pathologic basis of disease. 7th edn. Philadelphia: Saunders; 2004.
Craft_004.indb 610
decreased production of vasodilators, such as nitric
oxide, and increased production of vasoconstrictors,
such as endothelin.
Finally, insulin resistance (see Chapter 35) is common
in hypertension, even in individuals without clinical
diabetes mellitus.13 Insulin resistance is associated with
decreased endothelial release of nitric oxide and other
vasodilators. It also affects renal function and causes the
kidneys to retain sodium and water. Insulin resistance
is associated with overactivity of the sympathetic
nervous system and the renin-angiotensin-aldosterone
system. The pathophysiology of primary hypertension
is summarised in Figure 23-4.
Secondary hypertension
Secondary hypertension is caused by an underlying
disease process or medication that raises peripheral
vascular resistance or cardiac output. The condition is
more prevalent in younger people (< 30 years of age) and
those over 50 years of age.14 If the cause is identified and
removed before permanent structural changes occur,
blood pressure returns to normal. Examples include
kidney disease due to the retention of sodium and water
(see Chapter 30), adrenocortical hormonal imbalances
Environmental factors
Defects in vascular
smooth muscle growth
and structure
Vascular wall
thickness
Total peripheral
resistance
31/08/10 2:40 PM
 622 PART FOUR alterations to body maintenance
An increased serum concentration of LDL is a strong
indicator of coronary risk.26,27 Serum levels of LDL
are normally controlled by hepatic receptors that bind
LDL and limit liver synthesis of this lipoprotein. High
dietary intake of cholesterol and fats, often in combi-
nation with a genetic predisposition to accumulations
of LDL, results in high levels of LDL in the blood-
stream. Oxidation of LDL, its migration into the vessel
wall and phagocytosis by macrophages are key steps in
the pathogenesis of atherosclerosis (see Figure 23-10).
LDL cholesterol also plays a role in endothelial injury,
inflammation and immune responses that have been
identified as being important in atherosclerosis for-
mation.28 Aggressive reduction of LDL with diet and
cholesterol-lowering drugs, such as HMG-CoA reductase
inhibitors, more commonly referred to as statins, is asso-
ciated with a dramatic decrease in risk for coronary heart
disease.29
Low levels of HDL are also a strong indicator of
coronary risk and high levels of HDL may be more
protective for the development of atherosclerosis than
low levels of LDL.30 HDL is responsible for ‘reverse
cholesterol transport’, which returns excess cholesterol
from the tissues to the liver for metabolism — in
this way cholesterol is cleared out of the blood. HDL
also participates in endothelial repair and decreases
thrombosis.31 Exercise, weight loss, fish oil consumption
and moderate alcohol use can result in modest increases
in HDL. You will often hear reference to LDL as ‘bad’
cholesterol (atherogenic — promoting development
of atherosclerosis), while HDL is referred to as ‘good’
cholesterol (for protection from atherosclerosis).
Other lipoproteins associated with increased cardio-
vascular risk include elevated serum VLDL (triglycerides)
and increased lipoprotein (a). Triglycerides are associated
with an increased risk for coronary heart disease,
especially in combination with other risk factors such
as diabetes mellitus. Lipoprotein (a) is a genetically
determined molecular complex between LDL and a
serum glycoprotein called apolipoprotein A and has been
shown to be an important risk factor for atherosclerosis,
especially in women.
In order to understand how modification of the diet
can impact on the risk of developing atherosclerosis,
it is important to consider the relationship between
dietary fats and the lipid profile in the blood. The main
types of dietary fats that are more atherogenic are the
saturated fats, with the trans-fats also contributing. In
contrast, the dietary fats that can assist in protection from
atherosclerosis are the unsaturated fats (polyunsaturated
and monounsaturated; see the box ‘Health alert: the basics
on fats’). The National Heart Foundation of Australia
recommends that intake of saturated fats should be
Craft_004.indb 622
reduced and that the total energy of the diet obtained
from saturated and polyunsaturated fats should be 8%
and 8–10%, respectively. However, currently the average
Australian dietary intake comprises 12.7% saturated fats
and only 4.9% polyunsaturated fats.32
H E A LT H A L E R T
The basics on fats
Saturated fats are found in animal fats (butter, cheese, beef,
pork, lamb, chicken) and some tropical oils (e.g. palm kernel).
All saturated fats are not the same; some are stickier than
others. They consist of a long chain of atoms that take a longer
time to burn than shorter chained fats. The longer the fat
takes to burn, the stickier it becomes. Those fats that become
stickiest are more conducive to weight gain and heart disease.
Unsaturated fats consist of two types: monounsaturated
and polyunsaturated. Both contain essential fatty acids (EFAs),
but polyunsaturated fats have more.
• Monounsaturated fats are liquid at room temperature but
more solid when refrigerated. They are found in especially
high concentration in olive and canola oils, which are
high in oleic acid, a common monounsaturated fat.
Monounsaturated fats are known to lower LDL levels and
raise HDL levels. They are more stable in heat than other oils,
thus they are often used for stir-frying and baking.
• Polyunsaturated fats are liquid at any temperature and are
found in vegetable oils, soya, fish, walnuts, pumpkin seeds
and flaxseed oil. They contain both omega-6 and omega-3
EFAs in varying ratios. Today people are eating many more
omega-6 EFAs than omega-3. Too much omega-6 can
contribute to clot formation; omega-3 fats have the opposite
effect, so to reduce the risk of heart disease we need more
omega-3 and less omega-6. Omega-3 EFAs are found in
fish oil, flaxseed (and flaxseed oil), canola oil, walnuts,
pumpkins and green leafy vegetables. Soya contains both
omega-6 and omega-3. Populations that eat high amounts
of omega-3 EFAs have a lower risk of heart disease. Omega-6
EFAs are found in vegetable oils such as corn, safflower,
sunflower, cottonseed, peanut, sesame, grape seed, borage,
primrose and soya. Omega-6 EFAs have protective effects
only when they are combined with omega-3 EFAs.
Trans-fats are primarily found in artificially solidified
(hydrogenated) oils (e.g. margarine and vegetable shortening).
By becoming more solid they lose EFAs. They can raise LDL
levels and lower HDL levels. They also can raise lipoprotein (a)
levels, which increases the risk of heart disease. Trans-fats raise
blood-sugar levels and contribute to more weight gain than
the same amount of other fats. ‘Partially hydrogenated’
or ‘hydrogenated’ on a food label means the food contains
trans-fatty acids (e.g. cakes, biscuits, crackers, processed
cheese).
31/08/10 2:40 PM
 chapter 23 • alterations of cardiovascular function across the life span
Table 23-7 COMPLICATIONS FROM ACUTE MYOCARDIAL
INFARCTIONS
TYPE CHARACTERISTICS
Arrhythmias Disturbances of cardiac rhythm, which affect
90% of cardiac infarction patients
Caused by ischaemia, hypoxia, autonomic
nervous system imbalances, lactic acidosis,
electrolyte abnormalities, alterations
of impulse conduction pathways or
conduction abnormalities, drug toxicity or
haemodynamic abnormalities
Left ventricular Characterised by pulmonary congestion,
failure reduced myocardial contractility and
abnormal heart wall motion
Cardiogenic shock can develop
Inflammation of Includes pericardial friction rubs
the pericardium Often noted 2–3 days later and associated
(pericarditis) with anterior chest pain that worsens with
respiratory effort
Organic brain Can occur if brain blood flow is impaired
syndrome secondary to acute myocardial infarction
Transient ischaemic Occur if thromboemboli break loose from
attacks or stroke clots that form in the cardiac chambers or on
cardiac valves
Rupture of heart Caused by necrosis of tissue in or around
structures papillary muscles
Affects papillary muscles of chordae
tendineae cordis
Predisposing factors include thinning of
wall, poor collateral flow, shearing effect
of muscular contraction against stiffened
necrotic area, marked necrosis at terminal end
of blood supply and ageing of myocardium
with laceration of myocardial microstructure
Rupture of wall of Can be caused by aneurysm formation when
infarcted ventricle pressure becomes too great
Left ventricular Late (month to years) complication of acute
aneurysm myocardial infarction that can contribute to
heart failure and thromboemboli
Infarctions around Occur in those structures that separate the
septal structures heart chambers and lead to septal rupture
Associated with audible, harsh cardiac
murmurs, increased left ventricular end-
diastolic pressure and decreased systemic
blood pressure
Systemic May disseminate from debris and clots that
thromboembolism collect inside dilated aneurysmal sacs or from
infarcted endocardium
Pulmonary Usually from deep venous thrombi of legs
thromboembolism Reduced incidence associated with early
mobilisation and prophylactic anticoagulation
therapy
Sudden death Arrhythmias frequently causative, particularly
ventricular fibrillation
Risk of death increased by age more
than 65 years, previous angina pectoris,
hypotension or cardiogenic shock, acute
systolic hypertension at time of admission,
diabetes mellitus, arrhythmias and previous
acute myocardial infarction
Craft_004.indb 635
635
Myocardial infarction can occur in various regions
of the heart wall and may be described as anterior,
inferior, posterior, lateral, subendocardial or transmural,
depending on the anatomical location and extent of tissue
damage from infarction. Twelve-lead electrocardiograms
help localise the affected area through identification of
Q waves and changes in ST segments and T waves (see
Figure 23-26). The infarcted myocardium is surrounded
by a zone of hypoxic injury, which may progress to necrosis
or return to normal. Adjacent to this zone of hypoxic
injury is a zone of reversible ischaemia. Ischaemic and
injured myocardial tissue causes ST and T wave changes.
If the thrombus breaks up before complete distal tissue
necrosis has occurred, the infarction will involve only
the myocardium directly beneath the endocardium. This
type of myocardial infarction most often presents with
no elevation of the ST segment on ECG and therefore
is termed non-STEMI.58,59 It is especially important to
recognise this form of acute coronary syndrome because
recurrent clot formation on the disrupted atherosclerotic
plaque is likely, with resultant infarct expansion. If the
thrombus lodges more permanently in the vessel, the
infarction will extend through the myocardium from
endocardium to pericardium, resulting in severe cardiac
dysfunction. This usually presents with significant
ST segment elevation on ECG (STEMI). Often a charac-
teristic Q wave will develop on ECG some hours later.
An ST elevated myocardial infarction (STEMI) requires
rapid intervention to prevent serious complications and
sequelae.
Additional laboratory data may reveal leucocytosis,
elevated sedimentation rate and C-reactive protein, all
of which indicate inflammation. The blood glucose level
is usually elevated and the glucose tolerance level may
remain abnormal for several weeks.53 Hypoxaemia may
also accompany heart failure.
Immediate treatment
Acute myocardial infarction requires admission to
hospital, often directly into a coronary care unit. The
individual should be placed on supplemental oxygen and
given aspirin immediately. Pain relief is of the utmost
importance and involves the use of sublingual glyceryl
trinitrate and intravenous morphine. Continuous
monitoring of cardiac rhythms and enzymatic changes
is essential, because the first 24 hours after onset of
symptoms is the time of highest risk for sudden death.
Both non-STEMI and STEMI are managed with the urgent
administration of thrombolytics or by percutaneous
coronary intervention along with antithrombotics.47
Further management may include ACE inhibitors
and β-blockers. Individuals who are in shock require
aggressive fluid resuscitation, inotropic drugs (drugs that
31/08/10 2:40 PM
 642 PART FOUR alterations to body maintenance

PA E D I AT R I C S
ALTERATIONS OF CARDIAC mechanism of causation is often unknown. The
FUNCTION incidence of congenital heart disease is three to
four times higher in siblings of affected children
Congenital heart disease and chromosomal defects account for about 6% of
Congenital heart disease (present at birth) all cases of congenital heart disease. However, the
accounts for approximately one-third of all con- cause of most defects is multifactorial.72,73
genital defects and is the major cause of death in Congenital heart defects can be described with
the first year of life other than prematurity. The respect to three principal areas:
incidence varies according to the particular defect; 1 Anatomical defects include valvular abnormalities;
however, the overall rate is about 5 per 1000 live abnormal openings in the septa, including
births.1,71 Several environmental and genetic persistence of the foramen ovale; continued
risk factors are associated with the incidence of patency of the ductus arteriosus; and
different types of congenital heart disease. Among malformation or abnormal placement of the
the environmental factors are: great vessels.
1 maternal conditions, such as intrauterine viral 2 Haemodynamic alterations caused by these
infections (especially rubella), diabetes mellitus, anatomical defects consist of (a) increases or
phenylketonuria, alcoholism, hypercalcaemia, decreases of blood flow through the pulmonary
drugs (e.g. phenytoin) and complications of or systemic circulatory systems and (b) the
increased age mixing of pulmonary and systemic blood
2 antepartal bleeding through an abnormal communication that
3 prematurity (see Table 23-9).72,73 permits flow between the two circulatory
Genetic factors also have been implicated in the systems. The movement of blood between the
incidence of congenital heart disease, although the normally separate pulmonary and systemic
circulations is termed a shunt. Movement from
Table 23-9 MATERNAL CONDITIONS AND the pulmonary to the systemic circulation
ENVIRONMENTAL EXPOSURES AND (i.e. from the right side of the heart to the left
THE ASSOCIATED CONGENITAL HEART side of the heart) is called a right-to-left shunt.
DEFECTS Movement from the systemic to the pulmonary
circulation (from the left heart to the right heart)
CAUSE CONGENITAL HEART DEFECT
is a left-to-right shunt. Shunt direction depends
Infection on relative pressures and resistances of the heart
Intrauterine Patent ductus arteriosus, pulmonary and surrounding vessels.
stenosis, coarctation of aorta 3 The status of tissue oxygenation is gauged by the
Systemic viral Patent ductus arteriosus, pulmonary presence or absence of cyanosis. Cyanosis is a
stenosis, coarctation of aorta bluish discolouration of the skin indicating that
Rubella Patent ductus arteriosus, pulmonary the tissues are not receiving normal amounts
stenosis, coarctation of aorta of oxygen, a condition known as hypoxia.
Metabolic disorders Hypoxia may result from any disorder that
Diabetes Ventricular septal defect, cardiomegaly, prevents oxygen from reaching the body’s cells.
transposition of the great vessels Ischaemia, for example, is hypoxia from lack of
Phenylketonuria Coarctation of aorta, patent ductus blood flow. Some congenital heart defects that
(PKU) arteriosus cause hypoxia and therefore cyanosis involve
Drugs
a right-to-left shunt, which directs blood flow
away from the lungs (see Figure 23-31). These
Alcohol Tetralogy of Fallot, atrial septal defect,
ventricular septal defect
defects are commonly called cyanotic defects.
Congenital defects that do not cause cyanosis,
Peripheral conditions
or acyanotic defects, may involve a left-to-right
Prematurity Patent ductus arteriosus, ventricular shunt, which directs blood towards the lungs, or
septal defect
no shunt at all.

Craft_004.indb 642 31/08/10 2:40 PM

 600 PART FOUR alterations to body maintenance

Lymph nodes
As lymph is transported towards the heart, it is filtered FOCUS ON LEARNING
through thousands of bean-shaped lymph nodes 1 Explain how the lymphatic system is involved in fluid
clustered along the lymphatic vessels (see Figure 22-49). movements.
Lymph enters the node through several afferent lymphatic 2 Outline the pathway of lymph flow, from entering the
vessels, filters through the sinuses in the node and leaves lymphatic system to entering the cardiovascular system.
by way of efferent lymphatic vessels. Lymph flows slowly
through the node, which facilitates the phagocytosis of
foreign substances within the node and prevents them
from re-entering the bloodstream. (Phagocytosis is AGEING AND THE CARDIOVASCULAR
described in Chapter 12.) SYSTEM
A range of normal anatomical and physiological changes
A are seen in the ageing heart.17 In most cases, these changes
do not lead to the development of cardiovascular diseases,
From heart To venous To heart
but reflect general body trends leading to decline in
system performance towards the later stage of our life span. There
is a decrease in the number of cardiac myocytes, with an
increased proportion of collagen within the myocardium.
Lymph The heart valves become calcified and fibrous. The size of
vessel the lumen in the left ventricle decreases. Also, more fat
Arteriole is deposited around the heart. These anatomical changes
Venule lead to corresponding alterations in cardiac performance.
The effects of ageing on cardiovascular function are
summarised in Table 22-3.
Blood vessels become less compliant (or stretchable)
with age, so that changes in vessel diameter are restricted.

Table 22-3 CARDIOVASCULAR FUNCTION IN THE ELDERLY

Arterial Venous RESTING CARDIAC
capillaries capillaries DETERMINANT PERFORMANCE
Cardiac output Unchanged or slightly decreased
in women only
Lymphatic
capillaries Heart rate Slight decrease
B
Stroke volume Slight increase
Fluid Anchoring
Ejection fraction Unchanged
exchange filament
Afterload Increased
End-diastolic volume Unchanged

End-systolic volume Unchanged

Contraction Increased because of prolonged
Lymph relaxation
Cardiac dilation No change

Source: Gerstenblith G, Lakatta EG. Aging and the cardiovascular

Blood capillary system. In: Willerson JT, Cohn JN (eds). Cardiovascular medicine.
New York: Churchill Livingstone; 1995; Kaye D, Esler M. Sympathetic
neuronal regulation of the heart in aging and heart failure.
FIGURE 22-50 Lymphatic capillaries. Cardiovasc Res 2005; 66(2):256–264; Kenny RA, Ceifer CM. Aging
A Schematic representation of the lymphatic capillaries. B Anatomic and geriatric heart disease. In: Crawford MH, DiMarco JP. Cardiology.
components of microcirculation. London: Mosby; 2001.

Craft_004.indb 600 31/08/10 2:39 PM

 chapter 22 • the structure and function of the cardiovascular and lymphatic systems
In addition, there is narrowing of vessel lumen due to
development of atherosclerosis (described in detail in
Chapter 23). These changes, along with progressive fibrosis
that occurs with age, can substantially limit the movement
of vessel walls that is seen in younger ages. These changes
increase the tendency to develop raised blood pressure
with increasing age18 (see Figure 22-51). Increased blood
pressure (hypertension) and atherosclerosis are major
causes of cardiovascular pathophysiology, which are
discussed in more detail in Chapter 23.
FOCUS ON LEARNING
Discuss features seen during ageing on the heart and blood
vessels.
CHAPTER SUMMARY
The circulatory system
■ The circulatory system is the body’s transport
system. It delivers oxygen, nutrients and other
valuable substances throughout the body and carries
metabolic wastes to the liver, kidneys and lungs for
excretion.
■ The circulatory system consists of the heart and
blood vessels and is made up of two separate, serially
connected systems: the pulmonary circulation and
the systemic circulation.
■ The pulmonary circulation is driven by the right side
of the heart; its function is to deliver blood to the
lungs for oxygenation.
■ The systemic circulation is driven by the left side of
the heart; its function is to move oxygenated blood
throughout the body.
The structure of the heart
■ The heart consists of four chambers (two atria and
two ventricles), four valves (two atrioventricular
valves and two semilunar valves), a muscular wall, a
fibrous skeleton, a conduction system, nerve fibres,
systemic vessels (the coronary circulation) and
openings where the great vessels enter the atria and
ventricles.
■ The heart wall, which encloses the heart and divides
it into chambers, is made up of three layers: the
pericardium (outer layer), the myocardium (muscular
layer) and the endocardium (inner lining).
■ The myocardial layer of the two atria, which receive
blood entering the heart, is thinner than the
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601
200
150 Systolic
Pressure (mmHg)
Mean
100
Diastolic
50
0
0 20 40 60 80
Age (years)
FIGURE 22-51 Changes in systolic, diastolic and mean arterial
pressures with age.
The shaded areas show the approximate normal ranges.
Source: Guyton AC, Hall JE. Textbook of medical physiology. 11th edn.
Philadelphia: Saunders; 2006.
myocardial layer of the ventricles, which have to be
stronger to squeeze blood out of the heart.
■ Deoxygenated (venous) blood from the systemic
circulation enters the right atrium through the
superior and inferior venae cavae. From the atrium,
the blood passes through the right atrioventricular
(tricuspid) valve into the right ventricle. In the
ventricle, the blood flows from the inflow tract to
the outflow tract and then through the pulmonary
semilunar valve (pulmonary valve) into the
pulmonary artery, which delivers it to the lungs for
oxygenation.
■ Oxygenated blood from the lungs enters the left
atrium through the four pulmonary veins (two from
the left lung and two from the right lung). From
the left atrium, the blood passes through the left
atrioventricular valve (mitral valve) into the left
ventricle. In the ventricle, the blood flows from the
inflow tract to the outflow tract and then through
the aortic semilunar valve (aortic valve) into the
aorta, which delivers it to systemic arteries of the
entire body.
■ The heart valves ensure the one-way flow of blood
from atrium to ventricle and from ventricle to artery.
Heart sounds are due to closing of the valves at
slightly different times.
Fetal circulation
■ The fetal circulation is structurally different to that of
the adult, due to the umbilical cord, ductus venosus,
foramen ovale and ductus arteriosis. These structures
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 604 PART FOUR alterations to body maintenance
oxygen for use during the systolic phase of the
cardiac cycle.
The lymphatic system
■ The lymphatic vessels collect fluids from the
interstitium and return the fluids to the circulatory
system. The vessels of the lymphatic system run in
the same sheaths with the arteries and veins.
■ Lymph (interstitial fluid) is absorbed by lymphatic
venules in the capillary beds and travels through ever
larger lymphatic veins until it is emptied through
the right or left thoracic duct into the right or left
subclavian vein.
■ As lymph travels towards the thoracic ducts, it is
filtered by thousands of lymph nodes clustered
Tim is a 32-year-old engineer who started a job at
a new company one year ago. When he started his
new job, Tim realised that after being employed
with his previous company for 10 years, he had
allowed himself to become complacent with
many aspects of his life, including his health. He
decided to get fit again and slowly worked up to a
C A SE STUDY
comprehensive exercise regimen. He now exercises
for one to two hours per day and has a healthy
diet. He does not smoke, but he does enjoy regular
partying and drinks alcohol on weekends. His
height and weight are normal.
Tim recently volunteered for a research project
on exercise physiology and has been able to see a
range of data on his cardiac performance. During
the exercise phase of the project, Tim was required
to undertake vigorous cycling for 30 minutes while
he was attached to various monitors that assess his
ventilation and heart performance. He was unable
to drink fluid during the period of cycling.
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around the lymphatic veins. The lymph nodes are
sites of immune function.
Ageing and the cardiovascular
system
■ With increasing age, there is a tendency towards
replacement of normal structures with collagen and
fibrous tissue. Both the myocardium and heart valves
are affected.
■ With age, blood vessels lose their compliance, which
can increase the tendency to develop high blood
pressure (hypertension).
1 His cardiac output at rest was estimated to be 5.8 litres/
minute. How does this value compare with the average
value? Discuss what processes have led to his cardiac
output being 5.8 litres/minute.
2 Tim’s cardiac output during vigorous exercise was
28 litres/minute. How does this value compare with the
values discussed in question 1?
3 What would the circulating levels of antidiuretic
hormone (ADH) be in Tim’s blood by the end of the
30 minutes of exercise?
4 Discuss how secretion of renin would be altered at the
end of 30 minutes of exercise. What are the effects of
renin secretion?
5 Explain how the autonomic nervous system coordinates
blood flow to different organs during exercise. How
would this be different one hour after completing
exercise?
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 chapter 22 • the structure and function of the cardiovascular and lymphatic systems
R E VI E W QUESTIO NS
1 Draw the heart and systemic and pulmonary
circulations. Label the great vessels, heart
chambers, heart valves and whether blood is
oxygenated or deoxygenated.
2 Discuss why it is so beneficial for the fetus to have
structural specialisations to the cardiovascular
system. (Think about what the effects might be
on the mother if these specialisations were not in
place.)
3 Explain the phases of the cardiac cycle, ensuring
that you include pressure and volume changes
within the chambers.
4 Discuss why the coronary circulation is necessary
and how this circulation can be modified in order
to maintain adequate blood flow.
5 Outline the specialisations of the myocardium that
are unique to allow the function of the heart.
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605
6 Explain how action potentials generated in the
sinoatrial node lead to the coordinated contraction
of the whole heart.
7 Outline how the autonomic nervous system
modifies the functions of the cardiovascular
system.
8 Explain what might be achieved from being able
to alter preload, afterload, myocardial contractility
and heart rate.
9 Describe the effect that the renin-angiotensin-
aldosterone system has on blood pressure.
10 Outline the role that the lymphatic system has in
working with the cardiovascular system. Predict
what might happen if a lymphatic vessel were
blocked.
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