Cardiovascular
system
Cardiac form,
function. pathophysiology and management.
Introduction
The heart is a
hollow organ divided into four chambers. The upper chambers are termed atria and
the lower chambers ventricles. Blood from the venous circulation enters the
atria where it is collected before passing through the atrioventricular valves
into the ventricles. Ventricular contraction pumps blood out through the
semi-lunar valves into the arterial
system to perfuse the lungs and body. The heart is therefore a blood pump. If
for any reason the pumping action of the heart stops death will occur within
minutes. This is because the tissues of the body are dependent on the
circulation of the blood for their supplies of oxygen and nutrients.
The four
chambers are the right and left atria and the right and left ventricles.
Between the right atrium and ventricle is the tricuspid valve. The mitral or
bicuspid valve divides the left atrium and ventricle. Between the ventricles
and main arteries are the pulmonary arterial and aortic semi-lunar valves, (fig
1)
The three
layers
The energy for
the pumping action is generated by the heart muscle, this unique cardiac muscle
is striped or striated in nature
and termed the myocardium. As the myocardium must contract approximately 72
times per minute it uses a lot of nutrients and oxygen. As with all other
tissues these are supplied in the circulating blood. The first two arteries to
leave the aorta are the right and left coronary arteries which perfuse the
myocardium. Disease of these arteries is termed coronary artery disease and is
a common cause of death in the Western world.
The inner
layer of the heart is composed of smooth squamous epithelium. This allows the
smooth uninterrupted flow of blood through the heart. This inner lining also
covers the heart valves. The importance of this epithelium is highlighted by
the effect of it becoming infected, a condition termed endocarditis. Usually
caused by a streptococcus, this condition causes inflammation followed by
deposits of fibrin causing the build up of "vegetation", (1).
If this material is dislodged it will enter the circulatory system as emboli
which can lodge in the small arterial supply of any part of the body.
The other
layer of the heart is itself made up of two layers and termed the pericardium.
The inner layer is composed of serous membrane and the outer layer of tough
fibrous tissue. This allows the heart to expand and contract during the normal
cardiac cycle. The fibrous layer is protective and prevents the heart over
expanding. If fluid or blood collects under the pericardium the pressure can
embarrass the heart and may cause death. This condition is termed cardiac
tamponade, (2).
Blood flow
through the heart
The heart is
essentially two pumps. The left side pumps blood to the body and the right side
to the lungs. Blood is pumped to the lungs purely to be oxygenated. The
haemoglobin in red blood cells absorbs oxygen and transports it via the left
side of the heart to all the tissues of the body. Both sides of the heart contract
together, simultaneously pumping blood to lungs and body, (fig 2).
As the atria
contract the pressure of the blood they contain increases, this has the effect
of opening the atrioventricular valves allowing the blood to pass through into
the ventricles. As the ventricles begin to contract the pressure of the blood
in them increases. This causes the atrioventricular valves to close and the
semi-lunar valves to open. This prevents the regurgitation of blood from the
ventricles back to the atria and directs blood into the arterial system. The
valves are therefore passive structures which open and close in response to
pressure changes in the blood. They are prevented from opening in the wrong
direction by tendinous cords which are attached to papillary muscles which
extend from the inner cardiac wall.
The principle
of pressure changes within the heart opening and closing valves is applied in
external cardiac massage. This compresses the heart between the thoracic
vertebral column and the sternum. As the pressure in the heart increases blood
will open the valves and be forced through. As valves only allow the blood to
flow one way the circulation can only occur in a physiological direction.
Cardiac massage will generate a cardiac output which may be detected as a
central pulse. This will perfuse the vital organs of the body such as the
lungs, brain, kidneys and the heart itself. This can be maintained until a
normal cardiac rhythm is restored.
As both
atrioventricular valves close they make a sound referred to as a
"lub". The closure of the two semi-lunar valves makes a
"dub". These are termed the first and second heart sounds, so the
normal heart should make a lub dub, lub dub, lub dub. Additional sounds may be
abnormal and may be caused by
disturbances in the smooth flow of blood. An abnormal heart sound referred to
as a "whoosh" is often heard in septal defects where there is a
communication between the right and left side of the heart, (a "hole in
the heart"), (3). The resultant mixing of oxygenated and
deoxygenated blood reduces the efficiency of the circulatory system. In this
case some oxygenated blood is returned to the lungs and some deoxygenated blood
is pumped into the systemic circulation. Such conditions are usually congenital
and require surgical correction.
Systemic and
pulmonary circulation
The left
ventricle contracts and the blood is ejected through the aortic semi-lunar valve into
the aorta. As the aorta passed through the thorax and abdomen, arterial
branches leave to carry blood to all parts of the body. The arteries eventually
divide down into arterioles which in turn supply blood to the capillary systems
in all tissues, (except the lungs). After giving up oxygen and nutrients to the
tissues and collecting carbon dioxide and waste products the blood is returned
into venules (fig 3).These pass the blood into larger veins and eventually join
the vena cava.
The vena cava
empties blood directly into the right atria. From here blood passes through the
tricuspid atrioventricular valve into the right ventricle. This discharges
blood via the pulmonary artery semi-lunar valve into the pulmonary artery. The
right and left branch of this artery supply the two lungs with blood, perfusing
the pulmonary capillaries. During circulation through the alveoli the blood
gives up waste carbon dioxide and picks up oxygen. Returning blood from the
lungs enters the left atria via the pulmonary veins. When the right atria contracts
the blood passes through the mitral or bicuspid valve into the left ventricle
to complete one cycle, (fig 4).
The muscle
mass of the left ventricle is greater than that of the right. This is because the
pressure required to perfuse the body is greater than that needed to pump blood
to the lungs. A typical pressure in the systemic circulation is 120/80 mmHg
whereas in the pulmonary circulation it is 25/8 mmHg (4). The first
pressure is taken when the heart is contracting and referred to as the systolic
pressure. The second pressure is recorded when there is no active cardiac
contraction in between beats. This reflects the elasticity of the arterial
system and is termed the diastolic pressure.
The cardiac
cycle
The heart
contracts at a regular rate from about eight weeks after conception until the
death of the individual. The rate varies with the age of the individual from
about 140 at birth to around 110 at age two, 80 at age ten to around 70 in
adults.
The internal
conducting system
The cardiac
cycle is controlled by specialised
conduction tissue in the heart. Inside the right atrium is an area termed the
sino-atrial, (SA) node. This generates the initial impulse to stimulate the
myocardium to contract. This impulse spreads to both atrium stimulating their
contraction. The specialised conduction tissues are termed the internodal
tracts because they are between the SA node and the atrioventricular (AV) node.
The AV node collects the impulse from the atria and passes it on to the bundle
of His (or atrioventricular bundle) in the cardiac septum. This divides into
two forming the right and left bundle branch. Finally the impulse innovates the
ventricular myocardial muscle via the Purkinje fibres. This internal conducting
system allows the phases of a cardiac cycle to be co-ordinated, (fig 5), (5)
The PQRST
When the
myocardium is stimulated there is an electrical change in the myocardial muscle
associated with contraction. This electrical activity may be detected with
electrodes on the surface of the body. This is the principle of the
electrocardiogram. When this is done three characteristic electrical phases can
be clearly noted.
Firstly there
is a P wave. This is the electrical activity as detected on the surface of the
body as a result of the contraction of the artial myocardium. Secondly there is
the larger QRS complex caused by the contraction of the larger muscle mass of
the ventricular myocardium. Thirdly there is a T wave. This is not associated
with any muscular contraction but arises as the ventricular muscle returns to
an electrically resting state. Finally there is then a short gap before the
next atrial contraction. The normal cardiac cycle therefore has a PQRST in that
order, (fig 6). In health the occurrence of these phases of the cycle is
regular and the rate is between 60 and 100 per minute. If these three criteria
are met the individual is in sinus rhythm, ie. the cardiac rhythm is controlled
by the sino-atrial artial node, (table 1).
If the phases
of the cardiac cycle occur regularly and in the correct order at a rate of less
than 60 times per minute the rhythm is termed sinus bradycardia. This is normal
in people who are physically fit, (fig. 7). If the rate is over 100 and the
other two criteria are met it is a sinus tachycardia. A sinus tachycardia is of
course normal during exercise, (fig. 8).
The terms
P,Q,R,S and T do not stand for anything and have no intrinsic significance what
so ever. They are arbitrary names given to specified phases.
Coronary
arterial disease
The reason it
is so vital for nurses to have a knowledge of normal and abnormal cardiac
function is because coronary arterial disease is the main single cause of
premature death and disability in the Western world. In the UK cardiovascular
disease kills 350 000 people every year (6). These premature deaths
are arguably almost all preventable. The site of pathology is the coronary
arteries which perfuse the myocardium. The first two
vessels which leave the aorta are the right and the left coronary arteries
which sub-divide into other arteries which perfuse the capillaries of the
myocardium. The myocardium is an active muscular tissue and therefore requires
a constant supply of blood.
Fatty material
is deposited into the wall of the coronary arteries in an irregular way. In
general this has three effects. Firstly the deposited material reduce the lumen
of the artery, therefore reducing the volume of blood than can travel through
that section of artery. The effect of this is the tissue that particular artery
supplies receives less blood than
normal. This reduced blood supply is termed ischaemia. Secondly because the
fatty material is laid down irregularly blood may start to clot on the uneven
surface. This can build up and form a blood clot or thrombosis. This may
completely occlude the lumen of the artery leading to the effected tissue being
totally deprived off its blood supply. This is termed an infarction, the area
of tissue cut off from it is blood supply is the area of infarct. Thirdly the
wall of the artery may be weakened resulting in blood leaking from the artery,
this is termed an aneurysm, (table 2).
The fatty
material deposited into the wall of the arteries is referred to as atheroma,
the arteries are described as atheromatous. The disease process is correctly
termed atherosclerosis, (fig 9). The aetiology of atherosclerosis is the focus
of much debate, but some of the commonly accepted factors are given in table 3.
(7)
As health
educators nurses can help people to change the risk factors in their life
styles which contribute to the aetiology of CHD. This will reduce the risk of
the development of the condition. Nursing support often needs to be an on-going
process. Risk factors such as diabetes and hypertension are directly related to
the degree of control of these chronic underlying conditions. If they are well
controlled by diet, exercise and good medication compliance their pathogenic
effect can be largely negated. The question as to whether atherosclerosis is a reversible
process is currently under debate, however recent research seems to indicate
that with life style changes it is, at least partly, reversible, (8).
List
some lifestyle factors which you know of that may lead to atherosclerosis.
Diet
high in polysaturated fat and sugar
Lack
of water soluble fibre and vitamins caused by lack of fresh fruit and
vegetables
Smoking
Lack
of aerobic excecise, 20 - 30 minutes most days is recomended
Psychological
stress
Obesity
While
lifestyle factors are important in the development of atherosclerosis, they are
not the only factors. Genetic factors certainly play a part in the aetiology.
Coronary heart disease is also more common in children who have had low birth
weights and some researchers have postulated that there is a link to organisms
such as helicobacter and clostridia.
We have mentioned
that atheroma in the coronary
vessels can lead to angina and infarction.
List some other
conditions caused by arterial pathology which may affect other parts of the
body.
Stroke and
transient ischaemia attacks
Mesenteric
ischaemia
Peripheral
vascualar disease
Arterial leg
ulcers
Angina
Angina
pectoris or angina of effort is a pain of myocardial origin. Typically it is
described as a tight or crushing chest pain often referred into the left arm.
The severity of pain may vary from mild to very severe and there may be
numbness or weakness in the arms. The patient often suffers extreme
apprehension and fear of death. In angina of effort the atheromatous coronary
arteries can supply enough blood to the myocardium for normal function at rest.
However with exercise the work load, and hence oxygen requirement of the
myocardium increase. This results in myocardial ischaemia which causes the
pain. The situation is analogous to cramp in a leg muscle.
The pain
causes the individual to stop the exercise and usually passes off within a few
minutes. This is because at rest the oxygen consumption of the myocardium is
reduced and the reduced perfusion once again becomes adequate. The action of
drugs such as Glycerine Trinitrate is to dilate the coronary arteries and so
allow more blood to flow into the myocardium to prevent or treat the
hypoperfusion.
Patients should
be advised to avoid sudden strenuous exercise, especially after meals and in
cold weather. Heavy meals should be
avoided. If overweight advice should be given on weight reduction, this will
reduce the tissue mass the heart is required to perfuse with blood therefore
reduce myocardial work load and oxygen requirement. It is particularly
important for angina sufferers not to smoke. Smoking increases the amount of
carbon monoxide in the blood which reduces it`s oxygen carrying capacity.
Smoking is also likely to increase the amount of atheroma. Nicotine will have a
vaso-constricting effect on the coronary arteries and also make an infarct more
likely to occur. Anaemia should be recognised and treated. This will increase
the volume of oxygen which can be transported by a given volume of blood.
Emotion and excitement can also precipitate an attack.
If the lumen of the coronary artery is
narrowed or the coronary arteries spasm for any reason then there will be a
reduction in the amount of blood supply to the myocardium. This will result in
angina pectoris, the pain caused by myocardial ischaemia.
Describe
what is meant by the term angina.
Angina describes the pain
caused by myocardial ischaemia.
Angina is caused by
reduced blood supply to the heart muscle or more precisely by an imbalance
between myocardial oxygen demand and the amount of oxygen the myocardium is
receiving.
What are the
clinical features of this angina?
The pain is typically
`heavy` and `constricting`, it occures as a central chest pain which may
radiate into the left arm. It may also radiate through to the back, down to the
epitgastric region, into the right are and into the lower jaw. The pain may be
accompanied by anxiety and sweating
Myocardial
infarction
The pain of
myocardial infarction (MI) is typically described as severe, crushing, tight
and heavy. As in angina the pain is usually felt in the chest and often
radiates into the left arm. It may also be referred down to the epigastrium,
through to the back, up to the jaw and even sometimes into the right arm. Pain
is of sudden onset and may come on during exercise, rest or sleep. The pain
does not pass off at rest and is not relieved by nitrates.
The pain is
caused by an area of myocardium which is suddenly deprived of its blood supply
because of the formation of a thrombosis in the coronary arterial blood supply,
(fig 10). Streptokinase given shortly after an MI can dissolve the clot,
restoring the blood supply before the infarcted myocardium dies. Such
thrombolytic agents are now commonly used throughout the UK. Thrombolytics
should be given as soon as possible after the onset of symptoms to minimise
myocardial cell death. This comparatively new treatment offers the possibility
of a coronary thrombosis which does not result in a myocardial infarction.
As the pain is
severe diamorphine is usually given intravenously in hospital, this will also
have an anxiolytic effect. An antiemetic is given to prevent the nausea and
vomiting associated with opiate use. Psychological support is vital. If the nurse reduces the level of
patient anxiety the levels of circulating adrenalin will consequently be
reduced. As one effect of adrenalin is to increase the excitability of the
myocardium, allaying anxiety may reduce the probability of ventricular
fibrillation. As emergency intervention may be needed in initial management an
intravenous cannula should be inserted and kept patent. Much of the further
nursing management of an acute MI is based on the early recognition and
prevention of complications. Throughout all management and patient education
the individual and his or her significant others should be closely involved.
Complications
of Myocardial infarction
Arrhythmia
An infarcted area
of myocardium will rapidly start to die, as will any tissue deprived of a blood
supply. As the cells become increasingly embarrassed they lose the ability to
control the electrical potential difference across their cell membranes. Such
areas of infarcted tissue are therefore in an electrically unstable condition.
If they start to transmit these abnormal electrical signals to other healthy
areas of myocardium, cardiac contraction will become abnormal. The infarcted
area therefore becomes a site or focus for electrical activity. As the normal
focus for electrical activity is the SA node the new area is out of place, it
is therefore referred to as an ectopic focus.
When the
myocardial muscle attempts to respond to an ectopic focus the normal rhythm is
disturbed and becomes an arrhythmia. The most common life threatening
arrhythmia is a rapid uncoordinated contraction of the myocardium termed
ventricular fibrillation, (VF). In this arrhythmia there is no cardiac output
at all so the blood pressure is zero. This is termed a cardiac arrest. The
patient is collapsed with no central pulse If uncorrected death will occur in
about three minutes as the brain becomes increasingly hypoxic. The ECG will
reveal a characteristic pattern quite unlike sinus rhythm, (fig. 11).
Cardiopulmonary resuscitation will maintain some circulation until a definite
diagnosis is made and defibrillation carried out. If VF occurs it is usually in
the first few hours after the infarct. It may however occur within a few
minutes or even seconds. All patients with an MI should therefore be closely
observed on a cardiac monitor as soon as possible, usually for 24 hours. Full
resuscitation facilities should always be immediately available.
Heart block
If any part of
the internal conducting system is infarcted it will no longer be able to
transmit internal impulses. There are basically three degrees of severity of
heart block. In the most severs case it may mean that the ventricles are not
innovated to contract and a ventricular standstill result. If this occurs the
patient will usually require a temporary or permanent pace-maker to
artificially stimulate ventricular contraction, (9).
Cardiac
rupture
Sudden
exertion in the week after an infarction will increase the pressure of the
blood inside the heart. This may result in a breach of the weakened cardiac
wall causing fatal haemorrhage. With time the infarcted area will heal as
fibrous tissue forms in the infarcted area, this will seal the heart wall
allowing gradually increasing exercise. From this it is clear that patients
after myocardial infarction should not be subject to strenuous exercise in
initial management.
Heart failure
If the pumping
activity of the heart is compromised cardiac failure may develop. This usually
first effects the left ventricle leading to left ventricular failure, (LVF).
Heart failure may be acute or chronic and usually is a complication of
myocardial infarction or atrioventricular valve disease, (10).
If an area of
myocardium is infarcted then the pumping efficiency of the heart will be
reduced. This may result in some blood being left in the left ventricle after
contraction. When the atria empties into the ventricle some of the blood will
not be able to enter due to the presence of blood in the ventricle from the previous
contraction. This means some blood will be left in the left atria. This backlog
of blood in the atrial will restrict the emptying of the pulmonary veins
increasing the pressure of the blood in them. This will in turn dam back to the
pulmonary capillaries, increasing the pressure in their venous ends. This
increased hydrostatic (fluid) pressure, in the capillaries will reduce the
reabsorption of tissue fluid leaving free fluid in the lung tissues. This is
pulmonary oedema.
Typically such
patients suffer difficulty in breathing (dyspnea) when lying down, (orthopnea)
and have to sleep in a sitting position. This is because the fluid covers the
lung fields when the patient is recumbent, preventing gaseous exchange. Acute
LVF is life threatening and often diagnostic pink frothy sputum is
expectorated. The aim of management is to improve cardiac function and prevent the problems of the fluid
backlog. Fluid input and output should be closely monitored and no additional
salt should be given in the diet. Patients should be nursed sitting up or
leaning forward. Diuretics will usually be given to reduce the fluid overload
that develops. In cyanosis or respiratory distress oxygen supplementation may
be given. Diet should be light and easily digestible as large meals will
increase the gastrointestinal blood supply demand.
The term
congestive cardiac failure usually refers to right ventricular failure (RVF).
The backlog of blood will lead to congestion effecting all of the body, (except
the lungs). Systemic oedema in the tissue spaces and will be influenced by
gravity and collect in the feet and ankles, or sacrum if the patient is in bed.
The presence of oedema is a risk factor for the development of pressure sores.
The oedema increases the distance from the blood capillaries to the tissue
cells, this may adversely effect cell nutrition and oxygenation. Regular re-assessment and positional
change are therefore particularly important. The backlog of blood in the
systemic veins may be noted as distension in neck veins. This raised jugular
venous pressure is indicative of raised venous pressure.
Reduction of
physical activity is usually indicated as it reduces the demands placed on the
heart. Bed rest is sometimes prescribed for a few days to facilitate this. The
risk of deep venous thrombosis should be minimised by regular active and
passive leg exercises, and the possible use of elastic support stockings and
low dose subcutaneous heparin. (11). Alcohol should be avoided as it
reduces the strength of cardiac contraction.
RVF may
develop following left ventricular failure or more acutely as a consequence of
right ventricular dysfunction. As the congestion progresses all organs of the
body may become congested with blood leading to multiple organ failure, eg. so
called cardiac cirrhosis.
So in congestive cardiac
failure the heart if unable to maintain sufficient cardiac output in the
presence of normal or even increased venous return. This results in a backlog of blood in
the venous system which can cause congestion in all organs of the body. The
incidence of this condition is approximately ten per thousand in those over the
age of sixty five and approximately fifty percent of individuals with severe
failure die within two years.
List some
conditions of the heart or circulatory system which may give rise to congestive
cardiac failure.
Myocardial infarction
Cardiomyopathy
Vavular disease
The initial clinical
picture in congestive cardiac failure depends on the side of the heart first affected.
In right ventricular failure the backlog of blood starts in the right ventricle
and dams back into the right atria and from there into the into the vena cava
the rest of the systemic veins. This may mean that there is systemic venous
congestion.
List any effects
you can think of chronic venous congestion.
Increased pulmonary venous
pressure may lead to pulmonary oedema
Systemic venous congestion
may lead to congestion anf failure of almost any organ, eg liver failure.
It may also lead to oedema
of the legs
The second type of heart
failure is left heart failure, or left ventricular failure. Here, as the left ventricle is not
working properly the blood dams back into the left atria then into the
pulmonary arteries and into the lungs causing oedema in the lungs.
What clinical
feature may be caused by pulmonary oedema?
Difficulty in breathing,
especially when the patient to breath lying doen, (orthopnoea). This is due to
an accumulation of fluid in the lungs.
Which group of
drugs may be given to reduce the volumes of fluid in the body?
Diuretics, eg. frusamide
What other drugs
may be used in congestive cardiac failure?
Diuretics with
possible potassium suplement
Digoxin
ACE
(Angiotensin converting enzyme) inhibitors
Nitrates
Cardiac glycosides
Shock
The heart is a
pump and derives the energy to pump from the myocardial muscle. If a section of
this muscle dies it will not regenerate as muscle cells do not undergo mitosis.
The infarcted area will fibrose in time but will not be contractile and will
not contribute to cardiac pumping activity. The result will be a non
moving area in the myocardium, ie.
it will be dyskinetic. If the myocardium is no longer able to generate a
pumping pressure sufficient to perfuse the tissues of the body the state of
hypotension is termed cardiogenic shock. The term shock means a state of acute
hypotension.
This reduced
blood pressure will reduce the perfusion of the myocardium itself which may
lead to further reduced myocardial function. Hypoperfusion of the brain will
mean the patient feels dizzy when they sit up and they may faint. It is
important to allow patients to stabilise in a sitting position before standing
upright. Close support and observation should be given. Inadequate perfusion of
the kidneys may lead to oliguria or anuria leading to damage of the nephrons
termed acute tubular necrosis. If the reduced perfusion persists acute renal
failure will ensue. In order to closely monitor renal function the patient will
be catheterised with hourly urine volumes recorded. All fluid input and output
will be recorded and a balance calculated.
Other features
which may indicate the onset of cardiogenic shock include cool moist skin and
peripheral cyanosis, resulting from poor superficial perfusion. In hypotension
there is peripheral vasoconstriction to conserve blood to supply the vital
organs. Reduced perfusion of the brain may cause restlessness, anxiety, apathy
or lessening of responsiveness.
In
cases of coronary heart disease there may a thrombosis formed in the coronary
artery which would result in a area of myocardium infarction.
Describe
in your own words what is meant by the term myocardium infarction.
Myocardail infactrion
describes an area of infarct in the myocardium. This is an area deprived of a
blood supply. When the blood supply is cut off the area of muscle deprived
starts to die and will eventually necrose.
Myocardial Infarction
typically has an acute presentation and the person complains of severe pain.
Describe the nature
and distribution of the pain which you might expect to see in the case of acute
myocardial infarction.
The pain is typically very
severe and `heavy` and `constricting`, it occures as a central chest pain which
may radiate into the left arm. It may also radiate through to the back, down to
the epitgastric region, into the right are and into the lower jaw. The pain may
be accompanied by anxiety and sweating.
Unlike angina pain in
myocardial infarction does not pass off with rest
A myocardial infarction is
usually caused by a coronary arterial thrombosis.
What immediate
medical treatment may be given to reduce the amount of damage to the myocardium
following a coronary thrombosis?
The main line of treatment
is to give an aspirin at once and to administer thrombolytic therapy as soon as
possible.
After a myocardial
infarction there are several complications which may occur. One of these is due
to the area of infarcted myocardium starting to die, it may act as an ectopic
electrical focus and generate ectopic electrical impulses at a rapid rate.
What may these
ectopic electrical impulses cause in terms of cardiac arrhythmias?
Ventricular ectopics
Ventricular tachycardia
Ventricular fibrallation
Atrial flutter
Atrial fibrillation
In addition to cardiac arrhythmia,
because there is an area of dead muscle in the myocardium the heart may not be
able to pump as efficiently as it could prior to the infarction.
What condition may
be caused by reduced pumping capacity of the myocardium?
Cardiogenic
shock
Relationship
of pathophysiology to nursing observations
Temperature
Pyrexia occurs
as a response to infection or tissue damage. After myocardial damage there is
often a low grade pyrexia. This is due to the damaged tissue releasing pyrogens
which influence the hypothalamus and is not indicative of infection. However
viral or bacterial infection in the heart can lead to a pyrexia of infectious
origin. Inflammatory conditions may have the same effect. If an individual is
immobile pyrexia may indicate the onset of hypostatic pneumonia or possibly
deep venous thrombosis. Reduced peripheral temperatures may indicate reduced
tissue perfusion.
Pulse
The rate
rhythm and general quality of the pulse should be regularly assessed. A weak or
absent peripheral pulse may indicate poor cardiac output. A fast thready pulse
is usually caused by shock. Sometimes an abnormal cardiac rhythm may be felt in
the pulse such as the coupling of the beats in a so called bigeminal pulse.
Missed beats may indicate ventricular ectopic beats and an irregular pulse may
be caused by atrial fibrillation, (fig. 12). In routine situations the radial
pulse should be used, however in emergency situations a central pulse such as
the carotid or femoral should be palpated. If the systolic blood pressure is
below about 75 mmHg there will be no radial pulse palpable, however a systolic
of 50 mmHg will generate a palpable central pulse. The rate of the pulse will
indicate the presence of a tachycardia or bradycardia.
Blood pressure
Hypertension
should be detected and treated as it is a major aetiological factor in
atheroscleroses. This should form a routine part of any assessment in hospital
or community. As mentioned the damaged heart may not be able to sustain a
normal blood pressure. This means that regular blood pressure measuring can be
a useful parameter for monitoring the evolution of an individual`s condition.
Hypotension may also occur as a side effect of drugs such as beta blockers.
Respirations
Respiratory
distress may indicate the onset of pulmonary oedema. Short gasping respiration
often mean a pain is being caused by the respiratory effort. This may indicate
muscular skeletal chest injury, lobal pneumonia or possible a pericarditis.
Tachypnoea may indicate heart failure or pulmonary embolism. The general pallor
of the individual should be monitored, with particular reference to signs of
cyanosis.
Cardiac
monitor
A cardiac
monitor gives a continuous readout of the three lead electrocardiograph. This
allows the early detection of any arrhythmias. A nurse may observe a cardiac
arrest on the monitor and start taking appropriate action before the patient
loses consciousness. Most systems allow for the printing out of significant
rhythm strips. As it takes time and experience to learn the interpretation of
the ECG monitor they are usually used in coronary care units
Patient
reporting
Of course the
patient will report essential assessment data. This will include duration,
location radiation and severity of pain. Normally a "pain thermometer"
will be used to achieve consistency. Shortness of breath, palpitations and
anxiety may also be reported. It must be remembered that all cardiac patients
will be anxious, it is only the degree of anxiety which will vary.
Psychological depression is a danger which should be detected early as
effective treatments are available. Threats to self-esteem and changes to body
image are largely responsible for such affective changes.
Endocarditis
This is a condition
affecting the lining of the heart and it may be caused by a variety of
infecting organisms. For example streptococcus viridans or staphylococcus
aureus. The infection of the lining of the heart affects the heart valves and
this is a particular problem because fibrin and platelets, in combination with
the infective organisms accumulate on the valves of the heart. This
accumulation of abnormal material is termed vegetation. Emboli can break off
from this vegetation causing small areas of infarct in organs such as the
spleen, kidneys, myocardium or lungs.
Given that
endocarditis is an infection, what clinical features might you expect to see?
Pyrexia
Malase
In addition to these
features you have mentioned there may be heart murmurs.
Given that endocarditis
is an infection causes by bacteria suggest some possible treatments for the
condition.
Antibiotics
Rest
Given that
endocarditis is an infection suggest some possible investigations which may be
carried out.
Blood cultures to
determine the aetiological organism
Echocardiography to check
on valve function
Prophylaxis in endocardial
abnormalities
Patients at risk of
developing endocarditis should receive antibiotic prophylaxis before undergoing
procedures likely to result in bacteraemia, such as dental extractions or even
dental fillings. Patients at increased risk of developing valvular vegetation
include those who have had rheumatic fever in the past. Such patients should be
clearly identified so that appropriate prophylaxis may be offered prior to
potential bacteremia causing procedures.
* PQRST
in the right order
* PQRST
phases are regular * rate
between 60 and 100
Table. 1 The
three criteria for a normal sinus rhythm.
* ischaemia
* infarction * aneurysm
Table 2. The three
complications of atherosclerosis
* sedentary
life style
* high
fat diet * lack
of fruit and vegetables
* smoking * psychological
stress
* male
gender * age
* hyperlipidaemia
* obesity * hypothyroid
disease
* poorly
controlled diabetes mellitus * hypertension
* hereditary
Table 3.
Factors in the aetiology of coronary arterial disease
* arrthymias
* heart
block * cardiac
rupture
* shock * heart
failure
Table 4.
Possible complications of myocardial infarction
References.
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Joiner CL. Trounce JR. (1987) A short textbook of medicine, Unibooks,
Hodder and Stoughton, London.
2. Anderson
KN. Anderson LE. Glanze WG. (1994) Mosby`s dictionary, Mosby, St Louis.
3. British
heart foundation, (1986), Congenital heart disease, Heart information
series no. 5
4. Green JH.
(1974) An introduction to human physiology, Oxford medical publications,
London
5. Guyton AC.
(1991) Textbook of medical physiology, WB. Sanders Co. Philadelphia
6. British heart
foundation, (1992), The heart, Heart information series no. 11
7. British
heart foundation, (1992), Reducing the risk of a heart attack, Heart
information series no. 14
8. Hulley
SB. Newman TB. Grady D. Garber AM. Baron RB. Browner WS. (1993) Should we be
measuring blood cholesterol levels in young adults? JAMA. 269(11):1416-9, Mar 17.
9. British heart foundation, (1989),
Pacemakers, Heart information series no. 9
10. British
heart foundation, (1989), Valvular heart disease, Heart information series
no. 13
11. Kumar PJ.
Clark LM. (1987), Clinical medicine, Bailliere Tindall.