Shock
Shock is a life-threatening situation. In most cases, it is due to poor
tissue perfusion with impaired cellular metabolism, manifested in turn by
serious pathophysiological abnormalities.
Types
of shock
While there is some practical wisdom in the saying ‘shock means
haemorrhage, and haemorrhage means shock’, there are other causes of shock
with different features.
Vasovagal
shock
Vasovagal shock is brought about by pooling of blood in larger vascular
reservoirs (limb muscles), and by dilatation of the splanchnic arteriolar bed,
causing reduced venous return to the heart, low cardiac output and reflex
bradycardia. Consequently, the reduced cerebral perfusion causes cerebral
Psychogenic shock
Psychogenic shock immediately follows a sudden fright (e.g. bad news) or
accompanies severe pain (e.g. a blow to the testes). The expression ‘I nearly
died of fright’ reflects the danger of the uncorrected faint.
Neurogenic shock
Neurogenic shock is caused by traumatic or pharmacological blockade of
the sympathetic nervous system, producing dilatation of resistance arterioles
and capacitance veins (see below) leading to relative hypovolaemia and
hypotension. There is a low blood pressure, a normal or decreased cardiac
output, a normal pulse rate and a warm dry skin. Trauma to the spinal cord and
spinal anaesthesia lead to a systolic pressure of around 70 mmHg, which may be
corrected by putting the patient in the Trendelenburg position, the rapid
administration of fluids and or a vasopressor drug.
Hypovolaemic shock
Hypovolaemic shock is due to loss of intravascular volume by haemorrhage,
dehydration, vomiting and diarrhoea (e.g. cholera, acute enterocolitis). Until
10—15 per cent blood volume is lost, the blood pressure is maintained by
tachycardia
and vasoconstriction. Fluid moves into the intravascular space from the
interstitial space a ‘transcapillary refill’ which may exceed 1 litre in
1 hour in injured but otherwise fit patients. In addition, the venous
capacitance vessels constrict, pushing blood into the arterial system and
therefore compensating for the volume deficit.
Traumatic shock
Traumatic shock is due primarily to hypovolaemia from bleeding
externally (open wounds), from bleeding internally (torn vessels in the
mediastinal or peritoneal cavities, ruptured organs such as liver and spleen
or fractured bones) or by fluid loss into contused tissue or into distended
bowel. Traumatic contusion to the heart itself may cause pump failure and shock,
while damage to the nervous system or to the respiratory system results in
hypoxia.
Burns
shock
Burns shock occurs as a result of rapid plasma loss from the damaged
tissues, causing hypovolaemia. When 25 per cent or more of the body surface area
is burnt, a generalised capillary
leakage may result in gross hypovolaemia in the first 24 hours.
Endotoxaemia due to infection makes matters worse and large volumes of colloidal
and crystalloid fluids are required for resuscitation.
Cardiogenic
shock
Cardiogenic shock occurs when more than 50 per cent of the wall of the
left ventricle is damaged by infarction. Fluid overload, particularly when
using colloids, can lead to over-distension of the left ventricle, with pump
failure. The resultant high filling pressures exerted by the right ventricle
make fluid leak out of the pulmonary capillaries, thereby causing pulmonary
oedema and hypoxia. If an arrhythmia occurs this will reduce the pumping
efficiency of the heart, while hypovolaemia from excess sweating, vomiting and
diarrhoea will further diminish cardiac output.
Acute
massive pulmonary embolism from a
thrombus originating in a deep vein or an air embolus (more than 50 ml), if
obstructing more than 50 per cent of the pulmonary vasculature, will cause
acute right ventricular failure. This greatly reduces venous return to the
left ventricle, and cardiac output falls catastrophically causing sudden death
or severe shock.
Septic
(endotoxic) shock
Hyperdynamic (warm) septic shock. This occurs in serious Gram-negative
infections (see Chapter 5), for example from strangulated intestine,
peritonitis, leaking oesophageal or intestinal anastomoses, or suppurative
biliary conditions. At first, the patient has abnormal or increased cardiac
output with tachycardia and a warm, dry skin, but the blood is shunted past the
tissue cells, which become damaged by anaerobic metabolism (lactic acidosis).
The capillary membranes start to leak and endotoxin is absorbed into the bloodstream,
leading to a generalised systemic inflammatory state. The immediate and ready
treatment of the cause, including the drainage of pus, is vital to the recovery
of the patient at this stage (in strangulated hernia ‘the danger is in the
delay, not in the operation’).
Hypovolaemic
hypodynamic (cold) septic shock. This follows if severe sepsis or endotoxaemia
is allowed to persist. Generalised capillary leakage and other fluid losses lead
to severe hypovolaemia with reduced cardiac output, tachycardia and
vasoconstriction. The systemic infection induces cardiac depression, pulmonary
hypertension, pulmonary oedema and hypoxia which, in turn, reduce cardiac output
still further. The patient becomes cold, clammy, drowsy and tachypnoeic, but
still can be converted to hyperdynamic (warm) shock by the administration of
several litres of plasma or other colloidal solution. The similar use of crystalloid
solutions may give rise to systemic and pulmonary oedema because of the larger
volumes necessary.
Anaphylactic
shock
Penicillin administration is amongst the common causes of anaphylaxis.
Other causes include anaesthetics, dextrans, serum injections, stings and the
consumption of shellfish. The antigen combines with immunoglobin E (IgE) on the
mast cells and basophils, releasing large amounts of histamine and SRS-A
(slow-release substance-anaphylaxis). These
compounds cause bronchospasm, laryngeal oedema and respiratory distress
with hypoxia, massive vasodilatation, hypotension and shock. The mortality is
around 10 per cent.
Notes
on terms used
Resistance
arterioles are the small-calibre
vessels, 0.02—0.05 mm in diameter, containing abundant smooth muscle in their
walls, the tone of which is controlled by local humoral factors and the
sympathetic nerve fibres. The calibre of these small vessels gives rise to the
peripheral vascular resistance, controlling blood pressure and blood flow
through the capillary beds. The larger arteries merely serve to supply the
arterioles with blood.
Capacitance
veins comprise the entire venous network from the postcapillary venules to the
large-calibre veins in limbs, abdomen and thorax and which normally contain 70
per cent of the circulating blood volume. Although thin walled with relatively
little smooth muscle, sympathetic nerve stimulation contracts them, reducing
their diameter and emptying the blood into the arterial side of the circulation.
A
colloidal solution is one in which the
majority of solute particles has a molecular weight greater than 30 000. The
term includes all plasma solutions, including human plasma protein fraction (HPPF),
dextrans, gelatin (e.g. Haemaccel) and hydroxyethyl starch. Blood is not usually
included in this term.
Minute
volume ventilation is the volume of
air (or oxygen) which enters the patient’s lungs in 1 (each) minute, and is
the product of respiratory rate and tidal volume.
Hyperventilation
occurs when the patient is ‘overbreathing’ due to pain, anxiety or
shock, such that the arterial carbon dioxide tension (PaCO2) is
lowered from the normal 40 mmHg (5.5 kPa).
Aspects
of the pathophysiology of haemorrhage and shock
Low cardiac output is an early feature in shock, except for warm septic
shock and neurogenic shock. Vasoconstriction occurs in an attempt to maintain
perfusion pressures to the vital organs, such as the brain, liver and kidneys,
as well as the heart muscle itself. Venoconstriction pushes more blood into the
dynamic circulation whilst tachycardia helps to maintain a falling cardiac
output. The minute ventilation rises 1.5—2 times and the respiratory rate
2—3 times maintaining oxygenation (except in cardiogenic shock with
pulmonary oedema). The renal blood flow is reduced with consequent reduction in
glomerular filtration and urine output. The renin—angiotensin mechanism is
activated with further vasoconstriction and aldosterone release, causing salt
and water retention. Release of antidiuretic hormone (ADH) decreases the volume
and increases the concentration of urine. However, in early sepsis the patient,
although hypovolaemic, may produce inappropriately large amounts of dilute
urine (see below).
As
cardiac output falls, the hypotension and tachycardia cause poor perfusion of
the coronary arteries, and this, in conjunction with hypoxia, metabolic acidosis
and the release of specific cardiac depressants (endotoxaemia or pancreatitis),
causes yet further cardiac depression and pump failure.
The
cells become starved of oxygen, and anaerobic metabolism leads to lactic
acidosis. Eventually, the cell membranes cannot pump sodium out of the cells;
sodium enters the cells and potassium leaks out . Thus, the serum potassium is elevated. Calcium, however,
leaks into the cells lowering the serum calcium. Furthermore, the intracellular
lysosomes break down and release powerful enzymes causing further damage — ‘the
sick cell syndrome’.
The
platelets are activated in shock owing to the stagnation of blood in the
capillaries. Blood sludging with red cell aggregation may progress to the
formation of small clots and, indeed, to DIC. Several coagulation factors are
consumed (platelets, fibrinogen, Factor V, Factor VIII, prothrombin), and
troublesome bleeding may occur from needle puncture sites, wound edges and
mucosal surfaces.
Diagnosis
The prognosis of a shocked patient is related to the duration and
degree of the shocked state, therefore prompt diagnosis of the type of
shock is essential. It should be remembered that a thready and irregular pulse
can make the measurement of blood pressure inaccurate and misleading.
Intra-arterial pressure monitoring should be used. The ECG should be monitored
to detect any arrhythmias that may occur. A chest X-ray may reveal mediastinal
trauma or cardiac tamponade.
Central
venous pressure
The measurement of central venous pressure (CVP) and its response to a
small fluid challenge (200 ml of crystalloid or colloid) may assist in
distinguishing between cardiogenic shock and hypovolaemic shock, but it must be
emphasised that, in the seriously ill patient, the CVP is not a reliable
indicator of left ventricular function because of the wide disparity that can
exist between the left and the right ventricular functions.
Pulmonary
capillary wedge pressure
The pulmonary capillary wedge pressure (PCWP) is a better indicator of
both circulating blood volume and left ventricular function. PCWP is obtained
by a pulmonary artery flotation balloon catheter (Swan—Ganz). This can be
used to differentiate between left and right ventricular failure, pulmonary
embolus, septic shock and ruptured mitral valve, and can also be an accurate
guide to therapy with fluids, inotropic agents and vasodilators. It may also be
used to measure cardiac output by a thermodilution technique simply at the
bedside.
Measurement
of pulmonary capillary wedge pressure
This specialised procedure requires supervised training, practice,
patience and experience in interpreting the values measured and waveforms
indicated. Complications include arrhythmias, pulmonary infarction, pulmonary
artery rupture, balloon rupture and catheter knotting, in addition to the
complication from central venous cannulation. The catheter should not be left in
situ for more than 72 hours; if further haemodynamic monitoring is required,
a new catheter should be inserted.
Method.
Strict aseptic central venous cannulation should be performed (e.g. via right
internal jugular vein) and using the appropriate introducers, cannula and
guidewire, the catheter, flushed and wiped with heparin saline, introduced into
the right atrium. The balloon, inflated with 1.5 ml of air, should be advanced
slowly via the right ventricle into the pulmonary artery, checked by x-ray and
monitored by pressure tracing, which becomes characteristically flat when the
balloon wedges in a small branch to give the capillary pressure (indicating left
atrial pressure). When the balloon is deflated, the pulmonary artery pressure is
obtained. The balloon must never be reinflated in the absence of a normal
pulmonary artery waveform as this means that the tip alone is wedged and
reinflation might therefore rupture the pulmonary artery. Withdrawal of 2—3 cm
is mandatory until the waveform reappears and reinflation can be permitted.
The
transducer should be placed at the midaxillary point (zero reference point); the
normal PCWP is between 8 and 12 mmHg (10.5 and 15.5 cmH2O),
and normal pulmonary artery pressure is 25 mmHg systolic and 10 mmHg diastolic.
Clinical
monitoring
In summary, patient monitoring in shock should include:
• pulse;
• blood pressure (recording systolic and diastolic pressure, the pulse
pressure, using an intra-arterial line if necessary);
• heart rate and rhythm (cardioscope);
• respiratory rate and depth;
• CVP;
• PCWP in severe shock when the diagnosis is in doubt;
• urine output;
• serial blood gases and serum electrolyte measurements.
Method
of central venous catheter insertion (the Seldinger technique)
A commercially available intravenous catheter, made to proper
standards and of requisite length (20 cm), is passed into the right, or left,
internal jugular vein. A line is drawn between the mastoid process and the
sternoclavicular joint.
The carotid artery is palpated on this line and the internal jugular
vein lies immediately lateral to it at the midpoint of this line. The head-down
position is used to prevent air being sucked in (air embolus) and to distend the
vein.
Using
full aseptic technique, a 7cm needle, mounted on a syringe, is inserted
caudally at 45degree
to the vertical into the internal jugular vein, the
syringe removed and the soft end of the Seldinger wire passed through the needle
into the vein. The needle is removed over the wire, and the catheter, placed
over the wire, is passed into the vein. The wire is removed, and the catheter
sutured into position and covered with a sterile, transparent, self-adherent
dressing (e.g. Opsite 2000).
The
catheter tip should be positioned in the superior vena cava or right atrium
(confirmed radiologically at the first opportunity). Preceding every
measurement, the patency of the catheter is confirmed by checking for a swinging
movement of the saline column level in time with the patient’s respiration.
The patency of the catheter may be confirmed by lowering the saline reservoir
briefly to check the free reflux of blood in the connecting tubing. It must be
emphasised that the use of this method requires supervised training, skill,
practice and patience, also referring to the special manuals, because the
complications can be serious, for example pneumothorax, haemothorax, brachial
plexus and phrenic nerve damage, and carotid artery perforation. The catheter
must be removed when not required for CVP measurement, and should not be kept
in position as a matter of convenience for electrolyte or parenteral infusions
(the latter entering the pleural cavity or the mediastinum can be lethal).
The
alternative, subclavian (infraclavicular) approach can be used, but has a higher
incidence of complications (e.g. pneumothorax or haemothorax). The catheter may
be tunnelled subcutaneously to improve fixation for a long duration and to
reduce the incidence of septic complications.
A
third approach is the insertion of a longer (60 cm) catheter into the median
basilic vein in the antecubital fossa; the tip often does not reach the superior
vena cava or right atrium, and therefore may not give an accurate CVP
measurement;
however, it is useful for a central infusion of fluids or drugs.
Central
venous pressure measurement
A saline manometer for measuring central venous pressure should be used.
This has a sterile glass or plastic tube manometer against a centimeter scale; a
spirit level is used to set zero (0) to the midaxillary point or the
manubriosternal angle. A three-way stopcock allows isotonic saline: (1) to run
into the vein from the reservoir; (2) to fill the manometer; and (3) to exclude
the reservoir and to allow the fluid in the manometer to fall to the level of
the CVP.
The
catheter is connected to the saline manometer, and readings are taken of the
saline level with the zero reference point at the midaxillary level. The
normal is 5—8 cm; if the CVP is low, the venous return should be supplemented
by intravenous infusion, but not if the pressure is high. Readings with the zero
reference point at the midaxillary level should
Treatment
of shock
The management of all types of shock should be vigorous and dedicated.
The objectives are to increase the cardiac output and to improve tissue
perfusion, especially in the coronary, cerebral, renal and mesenteric vascular
beds. The plan of action should be based on: (1) the primary problem —arrest
of haemorrhage, draining pus, etc.; (2) improving ventricular filling by giving
adequate fluid replacement, for example human albumin solution or fresh frozen
plasma, in sepsis and burns; (3) improving myocardial contractility with
inotropic agents — dopamine, dobutamine, adrenaline infusions; and (4)
correcting acid—base disturbances, using molar sodium bicarbonate when the pH
of arterial blood is less than 7.2, and electrolyte abnormalities, especially
potassium and calcium levels.
In
endotoxic shock, once the haemodynamic status has been improved, full doses of the
appropriate antibiotics are given to treat the causal infection. The circulation
may be deluged with bacterial membrane debris which may intensify the endotoxic
insult to the patient. This may be ameliorated by giving specific gammaglobulins to bind the endotoxin; the antibiotic polymixin E may also
adsorb some of the endotoxins. This will reduce systemic inflammatory effects,
diminish capillary leakage and improve organ perfusion.
Diabetic
patients in endotoxic shock are in a precarious position. Careful monitoring and
control of their nutrition and insulin requirements are necessary under the
instruction of a clinician with a special interest in diabetes.
Vasodilators
(hydralazine, phentolamine, glyceryl
trinitrate infusions and chlorpromazine boluses) may be given provided the blood
volume has been corrected and cardiac depression treated such that the systolic
blood pressure is 90 mmHg or more. The indication is persistent vasoconstriction
with oliguria, high CVP or PCWP and pulmonary oedema. Such therapy will improve
cardiac output and tissue perfusion, and reduce the work done by the heart. It
must be emphasised that vasodilators can only be used with extreme caution and
full haemodynamic monitoring, because the sudden production of vasodilation
in a hypovolaemic or dehydrated patient can be followed by a catastrophic fall
in arterial blood pressure. These drugs should be given only in small
intravenous doses or infusions and only until the extremities become warm and
pink, and the veins are dilated and well filled.