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Understanding shock
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Understanding shock
NS54 Collins T (2000) Understanding shock. Nursing Standard. 14, 49, 35-39.
Date of acceptance: July 4 2000.
Understanding shock
Box 1. Estimated blood loss anaerobic metabolism, in which the production of lactic cardiac output and results in a low perfusion state.
in trauma fractures and pyruvic acids causes the body to develop a systemic Hypovolaemia normally results from a haemorrhage,
metabolic acidosis. Anaerobic metabolism is far less which can be either internal, such as bleeding from
Pelvis 3,000ml efficient than the normal aerobic metabolism, which the spleen, or external, for example, from trauma.
Femur 1,000ml
uses oxygen. Eventually, lactic acid builds up as a waste Other causes include loss of fluid from extracellular
Tibia 650ml
Abdominal injury 2,000ml product of anaerobic metabolism. This is harmful to the compartments caused by severe vomiting and
Thoracic injury 2,000ml cells and needs to be removed by the blood and diarrhoea, bowel obstruction, pancreatitis, peritonitis,
subsequently broken down in the liver; however, this burns and an excessive diuresis normally related to
process also requires oxygen. inappropriate diuretic therapy.
Compensatory stage In this stage, the body tries to Hypovolaemic is the most common form of shock.
intervene with physiological adaptations to attempt to Sometimes the cause of fluid loss can be clearly iden-
overcome the shock. In an effort to compensate for tified, as with severe arterial bleed, but sometimes the
the metabolic acidosis due to anaerobic metabolism, cause of the fluid loss is not obvious. For example, an
hyperventilation occurs (Adomat 1992). Hypotension average man could accumulate one litre or 20 per cent
is detected early by the aortic and carotid sinus baro- of the bloods circulatory volume in the gastrointestinal
receptors, which control blood pressure. This stimulates tract during a paralytic ileus and this might not be
the release of adrenaline and noradrenaline, which immediately identifiable (Alexander et al 1994). Patients
cause vasoconstriction, leading to an increase in both who have sustained trauma are extremely likely to
blood pressure and heart rate (Clancy and McVicar have hypovolaemia, as large blood losses occur around
1996). The adrenaline and noradrenaline cause fracture sites; for example, three litres of blood can be
vasoconstriction of the skin, kidneys, gastrointestinal lost with pelvic injuries (Skinner et al 1990) (Box 1).
tract and other organs and concentrate the blood supply In early hypovolaemic shock, the patients blood
to the heart and brain, as the brain is more susceptible to volume can be reduced by as much as 10-15 per cent
damage than the other organs. As general blood flow is before symptoms occur. This is primarily due to delays
reduced, the kidneys are especially sensitive; urine output in the body recognising the blood loss and imple-
is reduced and oliguria might well develop. menting the compensatory stage of shock that has
Progressive stage This is where the compensatory already been discussed. It is only when the compen-
mechanisms that the body has implemented to try satory mechanisms fail that the classic symptoms of
and combat shock start to fail. If the originating shock occur and it is imperative that the nurse identi-
problem, such as blood loss, has not been corrected, fies that the patient is in shock as early as possible to
the compensatory mechanisms that the body uses to optimise the patients outcome (Box 2).
intervene in shock will eventually fail. Due to the If blood loss continues, the patient will develop a
decreased perfusion of the cells, sodium collects tachycardia as a result of the catecholamines adrenaline
inside the cells, while potassium leaks out. As and noradrenaline that have been released to try to
anaerobic metabolism continues, this will increase the increase the cardiac output. The pulse will be notice-
bodys metabolic acidosis, causing the arteriolar and ably rapid, weak and thready due to the low blood
precapillary sphincters to constrict such that blood is flow in the body, despite an increased heart rate.
trapped in the capillaries (Alexander et al 1994). Due Generally, this is the earliest sign of shock, but heart
to this, the hydrostatic pressure will increase and, rate can also increase due to other unrelated factors,
combined with histamine release, this will lead to such as pain or stress, so the presence of a tachycardia
leakage of fluid and protein into the surrounding alone is not diagnostic of shock (Flavell 1994).
tissues (Alexander et al 1994). As this fluid is lost, the Vasoconstriction also occurs because of the
blood concentration and viscosity increase, causing increased secretion of catecholamines (adrenaline and
sludging of the microcirculation. The prolonged noradrenaline) due to the body concentrating the
vasoconstriction will also cause the vital organs to be blood flow to the essential organs of the brain and
compromised due to reduced perfusion of the organs. heart. The skin will look cold and clammy and the feet
Refractory stage At this stage, the vital organs have and fingers will be particularly affected. The nurse
failed and the shock can no longer be reversed. Brain should assess for vasoconstriction by testing the cap-
damage and cell death have occurred. Death will illary refill. This is done by applying pressure to the
occur within a few hours. patients fingernail and waiting for the colour to
return to the nail bed. If it takes more than two sec-
onds for the colour to resume, the patient has poor
Classification of shock
capillary refill, which indicates vasoconstriction.
The five types of shock produce a variety of signs and Hypotension is normally a later sign of hypovolaemia
symptoms and the treatment varies for each type. that appears only after the patient has lost 30 per cent
Hypovolaemic shock This occurs when circulating or more of his or her blood volume (Flavell 1994).
blood volume is reduced, which causes a reduction in There will also be a narrowing of the pulse pressure,
Understanding shock
which is the difference between the systolic and diastolic Cardiogenic shock This is characterised as left Box 2. Four classes of
blood pressures. This is due to decreased cardiac stroke ventricular failure of the heart itself, which results in hypovolaemic shock
volume and increased peripheral resistance (Alexander reduced tissue perfusion and impaired cellular activity
et al 1994). A decrease in urine output will occur: urine (De Jong 1997). This pump failure, which produces a Blood loss Observations
production provides a direct measure of blood flow and low cardiac output state, normally follows a
Class 1: Usually few
perfusion to the kidneys, as vasoconstriction of the renal myocardial infarction. This type of shock can also (Up to 15 clinical signs
artery in shock causes the blood to be directed away from occur following heart failure, cardiomyopathy, trauma per cent Compensatory
the kidneys to the heart and brain. Initially, the respira- or myocarditis (De Jong 1997). Due to the low cardiac blood mechanisms
tory rate and depth increases in response to the cellular output state, there is a reduction in arterial blood volume) are activated
to cope with
hypoxia, but as the shock progresses, the respiratory pressure. The baroreceptors then release both
blood loss
rate decreases and metabolic acidosis increases (Flavell noradrenaline and adrenaline, hormones that cause
1994). A change in mental status indicates decreased an increase in the contractility of the heart and also Class 2: Rapid, thready
cerebral perfusion and oxygenation and the patient cause vasoconstriction within the body. Due to the (15-30 per pulse; cool skin
might appear confused, restless or unresponsive. damage to the heart muscle, the increase in heart rate cent blood Urine output
volume) reduced
Treatment for the shock consists of treating the will probably do little to increase cardiac output. This
Confusion
cause. For example, if the patient is bleeding, the tachycardia can also be detrimental to the heart, as it Change in all
cause must be found and treatment given to stop the is being placed under more pressure and requires a observations,
bleeding, which might require emergency surgery. All greater oxygen supply to the heart muscle that is except for
patients in the acute phase of shock should be given already ischaemiac due to the shock. blood pressure,
which remains
100 per cent oxygen via non-rebreathe masks. As with hypovolaemic shock, the falling cardiac out-
stable
However, COPD patients should be closely monitored put and blood pressure cause poor perfusion of blood
for reduced respirations and O2 saturations. Regular to the tissues and eventually the cells are unable to Class 3: A dramatic
blood gases should also be taken. Oxygen saturations maintain cellular homeostasis. The resultant hypoxia (30-40 per deterioration
and blood gases need to be monitored for both oxy- causes widespread vasodilation due to lactic acidosis, cent blood in all
volume) observations
genation and for metabolic acidosis. Ideally, oxygen resulting in a further drop in blood pressure that the
Severe
saturation should be greater than 95 per cent, but this compensatory mechanisms are unable to prevent. tachycardia and
will not always be possible, particularly for patients Pulmonary oedema will eventually occur when the hypotension
with hypovolaemic shock. Two large bore cannulae pulmonary circulation and the right side of the heart
should be inserted for the rapid administration of fluids; also begin to fail. Despite recent advances in haemo- Class 4: Immediate
(More than threat to
the ideal replacement fluid is blood, as colloid and dynamic monitoring and drug therapy, the mortality
40 per cent patients life
crystalloid fluids will increase the circulating volume, but rate remains high, with 80 per cent of patients dying blood Drastic action
cannot transport oxygen and dilute the blood further. from cardiogenic shock (Alexander et al 1994). volume) and surgery
When patients are in shock it can be difficult to A patient in cardiogenic shock will have a fast, weak required
obtain IV access. Normally the anti-cubital fossa veins pulse and a systolic blood pressure below 90mmHg.
(American College of Surgeons 1993)
in the arms are the easiest to cannulate in shock. His or her skin will be cold, clammy and cyanotic. The
Other options may be an IV cut down, where the skin patient will have a urine output below 30ml/hour and
is surgically cut to expose the vein and then it is can- may be confused as a result of poor cerebral perfusion.
nulated or a central line may be inserted. Treatment involves supporting the heart and reducing
Vital signs should be monitored regularly, including the patients anxiety and pain. The patient should be
temperature, because hypovolaemia does predispose given 100 per cent oxygen via face maskand frequent
to hypothermia. It might not be possible to obtain a observation of vital signs is necessary, including blood
blood pressure reading, but if a peripheral pulse can gases, O2 saturations, blood pressure, frequency and
be palpated it is safe to assume that the patient has a depth of respirations, pulse, heart rhythm and temper-
blood pressure of at least 80mmHg (Buckley 1992). ature. Diamorphine is given for pain and the patient
The patients level of consciousness should be regularly might require inotropic support to increase the contrac-
assessed using the Glasgow Coma score (Ellis and tility of the heart, thus increasing its cardiac output.
Cavenagh 1992) and any deterioration in consciousness
should be reported immediately. TIME OUT 3
Compare hypovolaemic and
TIME OUT 2 cardiogenic shock and make a
Refer to Box 2. Imagine that list of the differences in
you have a patient who has treatment. How do you think
class 2 hypovolaemic shock and nursing care might differ for each?
has lost 15-30 per cent blood
volume following a trauma. Think Anaphylactic shock This type of shock is a severe
about the ways you might prevent any further allergic reaction in which an antigen-antibody
blood loss.
reaction occurs. There are many causes, including
Understanding shock
Understanding shock
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