Textbook of Surgery Roshan Lall Gupta
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ShockSURGERY 1

In 1940, Blalock defined shock as peripheral circulatory failure resulting from discrepancy in the size of the vascular bed and the volume of intravascular fluid. According to Simeone (1964) shock occurs when the cardiac output is insufficient to fill the arterial tree with blood under sufficient pressure to provide organs and tissues with adequate blood flow. In 1994 Parillo considered shock as a profound and widespread reduction in the effective delivery of oxygen and other nutrients to tissues leading to reversible, and if prolonged, to irreversible injury. The above definitions clearly reveal a shift in emphasis from the peripheral circulatory failure to failure of perfusion of organs and tissues at cellular level. The decreased tissue perfusion causes cellular hypoxia leading to anaerobic metabolism and cellular dysfunction. At the initial stages, compensatory mechanisms are evoked (neural, neurohumoral) as well as inflammatory cascades. The systemic inflammatory response (SIR) is activated and if exaggerated may itself contribute to injury through various pathways and cascades including leucocyte activation and release of oxygen-free radicals. These can then result in multi-organ dysfunction.
 
VARIOUS TYPES OF SHOCK
  1. Hypovolaemic shock is the result of depletion of circulating volume from haemorrhage, plasma loss or loss of extracellular fluid.
  2. Severe septic shock may progress to shock and multi-organ dysfunction.
  3. Cardiogenic shock failure of the heart following myocardial infarction is the best example of cardiogenic shock. A similar situation is seen in massive pulmonary embolism, where the right side of the heart comes under sudden strain.
  4. Neurogenic shock is caused by injury to the spinal cord or high spinal anaesthesia. Vasovagal shock is a type of neurogenic shock. It is a fainting attack brought about by intense pain or sudden fear.
  5. Anaphylactic shock is known to follow penicillin injection or administration of sera. The histamine like substances released may 2cause massive vasodilatation which causes hypotension and shock. There may also be bronchospasm, laryngeal oedema and respiratory distress.
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.
 
HYPOVOLAEMIC SHOCK
This is the most common form seen clinically. It is the result of depletion of circulating volume from haemorrhage, plasma loss, as occurs in severe burns or loss of the extracellular fluid, as occurs in high intestinal fistulas, vomiting or diarrhoea. In severe ileus or volvulus, hypovolaemia may result because of the fluid sequestrated in the bowel.
 
Pathophysiology
The loss of a proportion of circulatory volume results in diminished venous return to the heart. This reduces cardiac output which leads to a fall in arterial blood pressure. The fall in blood pressure is sensed by stretch receptors in the carotid sinuses and aortic arch, and there is an increase in activity of the sympathetic nervous system. The reflex increase in sympathetic activity is augmented by stimulation of peripheral (carotid and aortic bodies) and central (ventral surface of the medulla) chemoreceptors. Hypoxia is the main stimulus to the peripheral chemo-receptors, whereas changes in pH and CO2 have predominantly central effects.
The sympathetic response increases heart rate and myocardial contractility, and constricts arterioles and venules especially those in the cutaneous and visceral circulations. The cardiac output rises and together with the increased peripheral resistance elevates the arterial pressure. The venoconstriction by decreasing the capacity of the venous vascular bed promotes venous return to the heart, and also helps to sustain the cardiac output. Some degree of circulatory autoregulation may help to protect the renal, coronary and cerebral circulations.
There are some other mechanisms also towards the maintenance of circulation
  1. A reduction in renal blood flow lowers the afferent arteriolar pressure which increases the output of renin from the juxtaglomerular apparatus.
  2. This in turn leads to the formation of angiotensin which in addition to being a potent vasoconstrictor, liberates aldosterone from the adrenal cortex and thereby enhances tubular sodium reabsorption and hence fluid retention.
  3. Antidiuretic hormone (ADH) further helps in this conservation of fluid. ADH released from the posterior lobe of the pituitary is mediated by stimulation of low pressure baroreceptors (volume receptors) at the junction between the left atrium and the pulmonary veins.
Nevertheless, despite circulatory adjustments the cells become starved of oxygen, and anaerobic metabolism leads to lactic acidosis. The sustained hypoxia leads to development of 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. Several coagulation factors (platelets, fibrinogen, factor V, factor VIII, prothrombin) are consumed and troublesome bleeding may occur from needle puncture sites, wound edges and mucosal surfaces.
 
Clinical Picture
The shocked patient is classically described as pale, sweating, and with a rapid pulse. The level of consciousness is reduced, respiration is rapid and shallow, and blood pressure is steadily falling. 3However, these are advanced features of hypovolaemic shock. Significant deterioration of tissue perfusion occurs long before changes are detected by the relatively crude measurements of pulse and BP. These may be normal in the early stage and it is essential to detect other early changes in vital tissue perfusion.
The degree of hypovolaemia determines the clinical signs. In mild hypovolaemia (deficit < 20 per cent of blood volume), the dominant signs are manifestations of adrenergic discharge to the skin; cool, damp extremities, particularly the feet. The urine output and blood pressure in lying down position are normal. The patient may be thirsty or chilly. If a mildly hypovolaemic patient sits or stands, the pulse rate increases and blood pressure falls.
Moderate hypovolaemia (deficit of 20–40 per cent of blood volume) produces signs of adrenergic discharge to the skin and decreased urine output, reflecting the effects of ADH and aldosterone. The pulse rate is moderately elevated, and the blood pressure in lying down position may be normal.
Severe hypovolaemia (deficit < 40 per cent of blood volume) produces signs of adrenergic discharge to the skin, decreased urine output, rapid pulse and low blood pressure. The cerebral ischaemia may present with agitation and restlessness.
Various parameters to obtain a more accurate picture of the competence of the circulation are given as follows:
  1. The level of cerebral activity in a patient who has not sustained a head injury, and is not under the influence of drugs, is a valuable, if rather imprecise measure of tissue perfusion.
  2. Hourly urine output is particularly valuable and easier to estimate. It should be at least 30–50 ml per hour in an adult.
  3. Central venous pressure (CVP) is a more sensitive reflection of volume depletion than the arterial blood pressure. The normal range is from 3–5 cm of water above the manubriosternal angle in a supine patient.
  4. Other measures of tissue perfusion are less widely used but have their advocates.
    1. Ear oximetry is a simple non-invasive method of assessing oxyhaemoglobin saturation.
    2. The balloon-tipped flow directed Swan-Ganz catheter is useful in the long-term care of shocked patients in the intensive care unit. The device is rarely needed in the early management of hypovolaemia when the central venous pressure provides essential information simply and quickly. The Swan-Ganz catheter is inserted via the right internal jugular vein, and advanced through the right heart into the pulmonary artery where characteristic tracings confirm correct positioning. The pulmonary artery pressure is measured, as is the pulmonary capillary wedge pressure, which correlates well with left atrial pressure, providing a good indicator of the left ventricular and the diastolic pressure. A Swan-Ganz catheter is ideal for monitoring safe volume replacement in an injured patient who also has myocardial disease.
 
Investigations
  1. Baseline haemoglobin, packed cell volume (PCV), white blood count, blood urea nitrogen, and blood group and cross match.
  2. Arterial blood gases should be estimated (pH, pO2, pCO2).
  3. An ECG monitor should be in place and the serum electrolytes should be measured, especially if the patient has a history of renal or cardiac disease, or is on diuretics.
    4
 
Management
The aim is to increase the cardiac output and to improve the tissue perfusion. The plan should be based on (i) the primary problem, i.e. arrest of haemorrhage; (ii) adequate fluid replacement; (iii) improving cardiac function with inotropic drugs; and (iv) correcting acid-base disturbance and electrolyte abnormality.
The outline of treatment is as described here.
  1. Resuscitation In haemorrhagic shock resuscitation should begin with the establishment of an airway. This can usually be accompanied by hyperextending the neck and supporting the jaw. Supplement nasal oxygen is usually all that is needed. Some may require tracheal intubation and mechanical ventilation. External haemorrhage, if present, should be controlled, and preparation should be made to operate on patients bleeding internally.
  2. Fluid replacement Crystalloid solution, (e.g. Ringer's lactated solution) should be used for initial resuscitation. The lactate buffers the metabolic acidaemia of shock by absorbing hydrogen ion to form lactic acid. The lactic acid is then oxidised to carbon dioxide and water in Krebs cycle. Glucose should not be used in initial resuscitation because it may induce osmotic diuresis, which may further deplete patient's circulatory volume.
The severity of shock should determine the rate and amount of fluid given. Resuscitation should begin with a crystalloid solution even if blood is available. By restoring peripheral perfusion, the initial fluid bolus flushes into the circulation, products of anaerobic metabolism (which may be a myocardial depressant). Cold, acidotic, hyperkalaemic blood may even further damage the myocardium.
Actually, blood should be withheld until bleeding has been controlled to reduce the loss of transfused blood cells. Two litres of crystalloid solution should be given as fast as possible in patients in severe shock. Blood pressure usually returns to normal and becomes stable. Less severe shock requires proportionately less fluid. The fresh blood should be used as it minimises the coagulation abnormalities. Blood substitutes like plasma or dextran should only be used when whole blood is not available. If whole blood is available, dextran should not be used, as this may interfere with cross matching, inhibits clotting system, and encourages bleeding.
Serious hidden losses of blood into the pleural and peritoneal cavities from visceral or major vessel injury, or into the soft tissues and retroperitoneum cause profound shock. Exsanguination on this scale may warrant immediate surgery rather than a failed attempt at fluid replacement.
Guideline to fluid replacement A reliable guide to fluid replacement is the monitoring of central venous pressure (CVP). Its response to a fluid challenge may also help towards the diagnosis of the type of shock. A high CVP indicates cardiac failure due to overload. Hypovolaemia is indicated by a low CVP. Replacement of fluid can safely be undertaken until CVP returns to normal.
Positioning of the patient Positioning of the patient in shock is of considerable importance. Elevation of both legs while maintaining the patient in supine position may produce transient autotransfusion of pooled blood from the peripheral circulation.
An overall inflatable medical antishock trousers (MAST), enclosing the lower extremities and abdomen has been advocated for some injured patients in the hope that the cardiac output will be redistributed to more vital areas. The garment compresses veins in the lower limbs and abdomen, and displaces blood centrally; however, it also compresses the inferior vena cava and perhaps the renal and hepatic veins, and this hinders blood return. Although the garment causes blood to shift from subdiaphragmatic to supradiaphragmatic organs, this will already have been accomplished 5by adrenergic discharge, and some residual blood flow to the splanchnic organs may be essential to prevent late organ failure.
The efficacy of this device is, therefore, questionable. The diaphragm may be pushed into the chest and interfere with ventilation.
MAST should not be considered as a substitute for transfusion. However, this may “buy time” until adequate replacement is available. This is useful during patient transfer because of its ability to tamponade leaking vessels and splint fractures. Blood pressure should, however, be carefully monitored during slow deflation (as a rapid release of pressure would cause a sudden fall in blood pressure). Intravenous fluids must be given to correct any hypotension.
Sedation Sedation is important in relieving pain and to allay fright. Sedation should be given intravenously since it is not properly absorbed if given subcutaneously. Extra care should be taken while prescribing sedation in head injuries as it may depress respiration. In acute abdominal pain or catastrophe (perforated viscus, ruptured abdominal aneurysm) before diagnosis has been ascertained, it may mask the symptoms and signs, and then the diagnosis becomes difficult.
The use of vasopressor drugs is not recommended. They raise the blood pressure by increasing peripheral vascular resistance and decreasing tissue perfusion. However, inotropic drugs like dopamine and dobutamine may need to be used to improve cardiac action.
Successful resuscitation is indicated by warm, dry well-perfused skin, a urine output of 30–60 ml per hour, and an alert sensorium.
 
SEPTIC SHOCK
The septic shock can result either by gram-negative or gram-positive bacterial infection. The majority of sepsis that results in shock these days, is caused by gram-negative bacteria because the gram-positive infection has now been mostly controlled. Moreover, from the standpoint of shock, the gram-positive sepsis is much less dangerous.
The frequent source of gram-negative infection is from genitourinary, respiratory or intestinal tract, and the causative organisms are Escherichia coli, Proteus, Klebsiella, Bacteroides and Pseudomonas aeruginosa.
Gram-negative sepsis has assumed greater importance in the present era as the indiscriminate use of potent antibiotics has led to the development of virulent resistant organisms. Large hospitals are a major reservoir of such an infection which is easily transmitted from one patient to another.
The advent of major surgery due to the development of anaesthesia and other aids has made surgeons bold enough to operate on elderly and low-risk patients who have poor resistance to infection. Moreover, in the modern times the trauma on the road and elsewhere is on the increase, and the infection of the traumatic wound is an important source of infection. The use of steroids and anticancer therapy makes patients an easy prey to infection.
 
Pathophysiology
Endotoxins are constituents of the cell wall of gram-negative bacteria and are released mainly when bacteria die. They are mostly referred to as bacterial lipopolysaccharides (LPS).
A cascade of events, that is, activation of the complement, coagulation, fibrinolytic and kinin systems by endotoxin and other bacterial cell products with subsequent activation of platelets and neutrophils is considered to play a significant role in producing endothelial injury at the microvascular level. Endotoxins also cause the sudden release of endothelial derived relaxing 6factor and other vasoactive substances from endothelial cells. Macrophages are also stimulated, and release a number of mediators (interleukin-6, tumour necrosis factor, arachidonic acid metabolites and lysosomal enzymes).
Endothelial injury causes increase in microvascular permeability and transcapillary fluid loss. This fluid loss results in decreased venous filling with decrease in cardiac output, tissue perfusion and oxygen delivery. The initial loss of intravascular volume results in a decline in the central venous pressure and the cardiac filling pressure, indirectly represented by the capillary wedge pressure. The cardiac output is maintained initially by an increase in the heart rate. These early responses represent a neuroendocrine reflex designed to maintain cardiac and cerebral perfusion via peripheral vasoconstriction and reflex tachycardia. Later, renin-angiotensin and adrenocortical hormone release occurs. Further loss of intravascular volume results in a drop in cardiac output and a reduction in blood flow to different organs. With further volume shifts, cardiac and cerebral perfusion are maintained by selective reduction in flow to the renal and splanchnic areas, resulting in oliguria and mesenteric ischaemia. Beyond this, further compensatory mechanism would fail, and adequate cerebral and coronary perfusion can no longer be maintained. The decreased cardiac filling and output may be exacerbated by the direct myocardial depression in sepsis.
The hypotension and defects in perfusion are exacerbated by the peripheral vasodilation (decreased systemic vascular resistance) produced by the release of kinins, histamine, and other vasoactive peptides. The septic process also alters energy metabolism as a result of monocyte production of cytokines [tumour necrosis factor (TNF) and IL-I]. These cytokines are important mediators of increased caloric demands and a hypercatabolic state.
The decrease in capillary hydrostatic pressure during hypovolaemia and hypoperfusion produces a movement of fluid from the interstitial space to the intravascular space as one of the compensatory mechanisms to maintain intravascular volume. At the cellular level, hypoxia interferes profoundly with cell metabolism. There is derangement of cellular membrane ATPase dependent Na+/K+ transport. Potassium leaves the cells, sodium and water enter and cause cell swelling. These effects are sometimes termed the sick cell syndrome.
Sepsis is the major risk factor in the development of multiple organ failure syndrome. As the incidence increases with the severity and duration of sepsis, its prompt recognition, and vigorous treatment assumes importance.
Man's response to injury depends partly upon underlying factors that may contribute to the development of infection and thus to organ failure. Cirrhosis is associated with liver failure, immune deficiency with diabetes, malnutrition or because of administration of steroids or cytotoxic agents. In many cases, mechanical factors related to the operation itself serve to initiate or permit septic complications. The use of prophylactic antibiotics and mechanical or antibiotic preparation of the bowel may decrease these dangers, but anastomotic leaks, or other breaks in technique continue to produce disastrous consequences.
Although the exact pathophysiology of multiple organ failure syndrome is unclear, injury of the microvascular endothelium is a factor common to all. Neutrophils are potential mediators of microvascular injury. These cells adhere to vascular endothelium and produce an assortment of toxic agents (proteases and toxic oxygen products) for the destruction of bacteria. However, they act in a non-specific fashion and when activated systemically can also produce injury to the normal micro-circulation. In addition to adherence, neutrophil aggregation plays an important role in the occlusion of postcapillary venules during generalised activation, causing ischaemia.7
Endothelial cells exposed to ischaemia produce cytokines that may participate in and modulate the inflammatory response, including IL-1, platelet activating factor, platelet derived growth factor, and arachidonic acid metabolites.
The hypermetabolic state precipitated by major sepsis is associated with enhanced hepatic gluconeogenesis for energy production at the expense of lean body mass.
Untreated sepsis, fever, cardiopulmonary failure, and a continuing negative nitrogen balance in association with altered muscle mitochondrial function all lead to multiple system organ failure. This condition is manifested by stress ulceration, biochemical signs of hepatic failure and lethargy progressing to coma. Finally, a terminal complex of irreversible cardiopulmonary failure, renal failure and clotting disorders ensues.
 
Early Recognition of Gram-Negative Sepsis
An early recognition of gram-negative infection can help in its control and this would prevent development of shock to a stage when no treatment may succeed. At times, the onset of shock may be abrupt and may coincide with the signs and symptoms of sepsis, or it may take several hours and days to appear. The initial signs of gram-negative sepsis are:
  1. Chills
  2. Elevated temperature above 101°F
  3. Hyperventilation. Mild hypoxia with compensatory hyperventilation and respiratory alkalosis are early signs of shock. This hypoxia may be due to arteriovenous shunting in lung due to perfusion of non-aerated part of the lung
  4. Oliguria
  5. Altered sensorium. It is worth emphasizing that development of mild hyperventilation and altered sensorium may be the earliest signs of gram-negative infection
  6. The white blood count is raised except in very ill patients or in those receiving immunosuppressants
  7. The falling platelet count may be an early sensitive indicator of gram-negative sepsis. Platelet aggregates are produced and subsequently trapped in micro-circulation. A fall in platelet count (on serial study) below 1,50,000 suggests the presence of gram-negative sepsis and measures to find and eradicate the source of infection should be undertaken. Rarely, a sudden fall in platelet count may be the manifestation of disseminated intravascular coagulation (DIC), a syndrome known to be initiated by several stimuli including bacterial endotoxins as mentioned earlier.
In gram-negative sepsis, depending upon the previous volume status of the patient, two distinct types of shock may occur—(i) hyperdynamic type, and (ii) hypodynamic. In hyperdynamic type the signs are:
  1. Hyperventilation
  2. High central venous pressure
  3. High cardiac output
  4. Alkalosis
  5. Oliguria
  6. Profound hypotension
  7. Warm dry extremities
  8. Low peripheral resistance.
The hyperdynamic shock is typically seen in a young female with normal volume status and who has been previously healthy and had septic abortion. It has been suggested that its treatment 8should include measures to further increase the cardiac output and appropriate antibiotic therapy along with early surgical drainage. However, if the control of infection is delayed, the patient may pass into an acidotic phase with low cardiac output and further cellular damage. This may not respond to treatment.
The hypodynamic septic shock is seen in patients who are already hypovolaemic with evidence of third space loss prior to the septic process, e.g. gangrenous intestinal obstruction, mesenteric thrombosis, and/or peritonitis. The hypodynamic shock is recognised by:
  1. Low central venous pressure
  2. Low blood pressure
  3. Low cardiac output
  4. Increased peripheral resistance
  5. Oliguria and
  6. Cold cyanotic extremities.
These patients, if seen early, are also alkalotic and would respond favourably to treatment. In the absence of obvious cardiac pump failure, a prompt volume replacement often increases cardiac output, and a more favourable hypervolaemic circulation may develop. If treatment for combating sepsis is delayed or is not successful, the patient has cardiac and circulatory failure with low fixed cardiac output and a resistant metabolic acidosis. This has very poor prognosis.
 
Management
It must be made clear that an established septic shock is mostly fatal. The only way to reduce mortality is by prompt recognition and treatment of infection prior to the onset of shock. The outline of management of an established septic shock is detailed below.
Patient should preferably be treated in an intensive care unit where direct arterial pressure as well as central venous pressure is monitored. It is better, however, to measure pulmonary wedge pressure by Swan-Ganz catheter, urine output is measured, and arterial and central venous blood gas estimations are done.
A thorough search for the source of infection is made while keeping the patient supported with adjunctive treatment. If it is possible to drain the infective process, it should be done soon to stabilise the patient's condition. The drainage may be done under local or general anaesthesia.
The primary goal of treatment is to restore the microcirculatory perfusion. The assurance of adequate delivery of O2, the most vital substrate, is of primary importance. The maintenance of an adequate airway and ventilation, including the administration of supplemental O2 is advisable. An early development of adult respiratory distress syndrome (ARDS) may require the use of positive end expiratory pressure.
The cardiac output should be increased by volume infusion. Resuscitation should begin with an intravenous infusion of Ringer lactate (20 ml per kg) as a bolus. Further fluid administration is dictated by the haemodynamic response to this initial infusion, that is restoration of cerebral status, arterial pressure and urinary output. If adequate perfusion is restored maintenance fluid may be all that is required. If the duration and severity of shock are severe, large volume infusions are required. Blood or blood products may be necessary to restore adequate perfusion and oxygen delivery. As there is a tenuous balance between the need for replacing and the harmful effects of fluid overload, properly interpreted central venous pressure helps in knowing the ability of the right heart to receive and pump blood. The use of Swan-Ganz catheter to guide volume infusion therapy may also be invaluable in the management of sepsis.9
Treating endotoxaemia Endotoxin is the potent activator of various cellular and humoral pathways involved in the generalised inflammatory response. It was presumed that endotoxin core antibodies for gram-negative bacterial endotoxins may help to reduce organ failure. However, the results have been inconclusive.
Use of drugs in septic shock The use of steroids in shock is controversial, but when used in large doses would improve the heart function, and produce mild peripheral vasodilatation. It has also been suggested that steroids protect cells from the effect of endotoxins, e.g. by stabilising the cellular and lysosomal membrane. A short-term high dose steroid therapy is associated with almost no known complication, and can be safely recommended for most cases of shock.
There is evidence to suggest that arachidonic acid metabolites play key role in the pathogenesis of multiple organ dysfunction, both protective (e.g. leukotrienes and thromboxane). Cyclo-oxygenase inhibitors (which are nonsteroidal anti-inflammatory drugs) have also been shown to improve survival in animal models of sepsis.
Volume resuscitation alone may be insufficient to restore arterial pressure and perfusion because of low systemic vascular resistance. When this occurs, use of cardiotonic and vasoactive drugs may be beneficial in improving mean arterial pressure and cerebral and coronary perfusion. Dopamine in doses of 2–10 μg/kg per minute, has inotropic as well as selective vasodilating effects on the renal and splanchnic circulation. Dopexamine is a synthetic catecholamine with similarities to dopamine. It causes vasodilatation in the renal, splanchnic and coronary circulations. It also causes vasodilatation in the skeletal muscle beds and the pulmonary circulation. Dopexamine improves cardiac performance in septic shock, but also increases the heart rate and decreases the systemic vascular resistance. Dopexamine appears to be most useful in patients with acute heart failure who benefit, not only from its inotropic properties, but also from its vasodilation.
Vasopressor drugs are not useful and may even be harmful due to their vasoconstrictor action. The heart action does certainly improve with vasopressors, but now there are better drugs available for improving the cardiac function.
Vasodilators such as phenoxy-benzamine have enjoyed popularity, but its efficacy was based on canine experiments, and it has not been possible to translate this experience in the human septic shock.
Digitalis is not favoured except in the very old and those with congestive heart failure.
Pulmonary therapy In sepsis, there may be endothelial damage to the pulmonary capillaries with resultant pronounced alveolar injury, interstitial oedema and haemorrhage. The inadequate lung function in many cases of sepsis with shock would require maintenance of a controlled airway and an assisted ventilation. The ventilatory assistance may not, however, be necessary if initial therapy against sepsis and shock is commenced early.
 
CARDIOGENIC SHOCK
Cardiogenic shock can occur with massive myocardial infarction, severe valvular heart disease, or arrhythmia. A similar situation is seen in massive pulmonary embolism, where the right side of the heart comes under sudden strain.
In cardiogenic shock, the heart fails to pump blood. The left ventricle mainly fails, there is overdistension of the right ventricle with a consequent increase in back pressure in the pulmonary capillaries. This leads to pulmonary oedema and hypoxia. The diagnosis is usually made on the basis of a known history of cardiovascular disease in a patient in shock with distended neck veins, 10peripheral oedema, an enlarged and tender liver, rales, ECG signs of ischaemia and an enlarged heart on X-ray.
 
Treatment
Treatment of cardiogenic shock consists of:
  1. Opioids to relieve pain and provide sedation. They are especially effective in treating cardiac failure after myocardial infarction
  2. Diuretics, by decreasing afterload alleviate peripheral and pulmonary oedema
  3. Inotropic agents improve cardiac contractility (without increasing heart rate too much—an inotropic like dopamine or dobytamine in low doses
  4. Mechanical support to the heart may be provided in selective patients with severe reversible left ventricular dysfunction by an intra-aortic balloon. It should only be used if a Swan-Ganz catheter is in place.
 
NEUROGENIC SHOCK
Neurogenic shock is associated with stress, spinal injury, or a high spinal anaesthetic. Such shock is primarily due to blockade of sympathetic nervous system, resulting in loss of arterial and venous tone with pooling of blood in the periphery.
The heart does not fill normally and the cardiac output falls. The patient is hypotensive with warm dry skin and normal pulse rate.
Vasovagal or psychogenic shock is also a part of neurogenic shock. This is a fainting attack brought about by intense pain or sudden fear. Due to sudden decrease in peripheral vascular resistance, there is pooling of blood mainly in limb muscles causing reduced return to the heart. The reflex vagal action produces bradycardia. The cerebral hypoxia due to reduced blood supply may cause unconsciousness. The onset is alarming, but the recovery is rapid. As stated earlier, the clinical picture is quite different from hypovolaemic shock. While blood pressure is low, the pulse rate is slower than normal and is accompanied by dry, warm and flushed skin.
The diagnosis rests on knowledge of the circumstances preceding the onset of shock and on the physical examination.
 
Treatment
Treatment consists of volume expansion with crystalloid solution (Hartmann's) to fill the expanded intravascular space. Neurogenic shock is the only type in which vasoconstrictors are useful. The goal is to increase blood pressure to the point that coronary perfusion is sustained. Trendelenburg's position can also be temporarily useful. Short-term steroids may also be useful.
 
ANAPHYLACTIC SHOCK
Anaphylactic shock has been known to follow penicillin injection or administration of serum. The antigen combines with immunoglobulin E (IgE) on the mast cells and basophils release large amounts of histamine and SRS-A (slow release substance-anaphylaxis). These substances may cause bronchospasm, laryngeal oedema and respiratory distress. This is aggravated by massive vasodilatation which causes hypotension and shock.
Aqueous epinephrine, 0.5–1 ml of 1:1000 solution should be given intravenously. A repeat dose may be given in 5–10 minutes followed by 5–20 mg of diphenhydramine slowly intravenously. 11Administration of corticosteroids and supportive measures such as oxygen administration, volume expanders and pressor agents are required in case of shock.
FURTHER READING
  1. Abel FL: Myocardial function in sepsis and endotoxin shock. Am J Physiol 257:1265, 1989.
  1. Rackow EC et al. Cellular oxygen metabolism during sepsis and shock. JAMA 259:1988–89.
  1. Saadia R, Lipman J: Multiple organ failure after trauma. BMJ 313:573, 1996.
  1. Thal AP, Wilson RF: Shock. Curr Probl Surgery 1965.
  1. Tinker J, Browne DRG, Sibbald WJ: Critical Care Standards, Audit and Ethics. Edward Arnold  1996.