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 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 hypoxia and unconsciousness, but prostration and reflex vasoconstriction so increases the venous return and cardiac output as to restore cerebral perfusion and consciousness. It must be remembered that if the patient is maintained in an upright or a sitting position (e.g. in a dental chair) permanent cerebral damage will occur.
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 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 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 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 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 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.
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.
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.
In summary, patient monitoring in shock should include:
• 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;
• 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 shouldnever exceed 10; if the readings are taken at the manubriosternal angle (angle of Louis), as they may have to be in a surgically draped patient, the range is 3—4 cm lower than midaxillary readings.
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.
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