Xing Meng Emergency Center Of The First Affiliated Hospital Of Zhengzhou University,zhengzhou
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Xing Meng Emergency Center of the First Affiliated Hospital of Zhengzhou University,Zhengzhou
1
1. Definition Shock is a emergency and fatal syndrome which results from poor tissue perfusion and tissue hypoxia from acute hemodynamic disturbance , leading to multiple organ dysfunction, moreover organ failure, and death. This syndrome is characterized by hypotension, pallor, cold clammy skin, alterations in mental status and reduction of urine formation. 2
2. Mechanisms A deficit in tissue perfusion can be caused by four major mechanisms: 2.1 hypovolemia; 2.2 cardiac failure; 2.3 peripheral distributive defects; 2.4 vascular obstruction.
3
2.1 hypovolemia Hypovolemia due to hemorrhage, plasma loss or extravasation of electrolytes and water results in a critical reduction of venous return to the heart, and therefore of cardiac output.
4
2.2 cardiac failure Cardiac contractility reduced by myocardial infarction,bacterial endotoxins or cardiac-depressant drugs and cardiac dysrhythmias (both tachycardias and bradycardias) ,can lead to a reduced cardiac output.
5
2.3 peripheral distributive defects Impaired peripheral distribution caused by an imbalance between precapillary sphincter and venular tone,or by the openingup of arteriolovenular communications, leads to tissue hypoxia.
6
2.4 vascular obstruction High-resistance shock is associated with intravascular sequestration of blood in the venous capacitance circuit. Any major obstruction to the circulation in the heart, major vessels or microcirculation also leads to failure to tissue perfusion.
7
3. Clinical manifestations The clinical syndrome of shock can develop over the course of a few minutes or several hours, depending on the cause; all systems may be affected.
8
3.1 Cardiovascular system Early Blood pressure Heart rate Cardiac output
N or ↓ N or ↑ N or ↑
Lately ↓ ↑ ↓
9
3.1.1 The blood pressure initially may be normal or only slightly decreased, because of compensatory vasoconstriction.Late in shock, both blood pressure and cardiac output are markedly reduced. 3.1.2 Tachycardia is usually present from the start, unless heart block is an etiological factor. 3.1.3 The peripheral pulses become thready or may be absent.
10
3.1.4 Cardiac dysrhythmias are common late in shock and are caused by hypoxia, metabolic disturbances and circulating cardiac toxins. 3.1.5 The ECG frequently shows signs of ischemia, ST depression and flattening of the T waves. 3.1.6 The CVP can initially be high in cardiogenic and obstructive shock,low in hypovolemic shock, and normal or low in bacteremic shock. 11
3.1.7 An increase in the PCWP in the presence of a low cardiac output is indicative of severe left ventricular failure. 3.1.8 The skin is a visible monitor of the state of the peripheral circulation. As shock develops, the patient becomes clammy and pale with peripheral cyanosis.The skin may feel cold,despite a high core temperature.
12
3.2 Respiratory system
Early Tachypnea Hyperpnea
Lately Tachypnea Laboured breathing Central cyanosis 13
3.2.1 Tachypnea and hyperpnea are present early in shock ， occuring in response to metabolic acidosis and hypoxemia. 3.2.2 Respiratory insufficiency has been found to be present in 62% of a series of patients with proved Gsepticaemia.
14
3.2.3 An increase in lung water leads to reduced compliance and impaired gas exchange. 3.2.4 Central cyanosis may be present. 3.2.5 The lung signs are nonspecific.On auscultation the lung may sound clear, or there may be widespread crepitations and zones of diminished air entry.
15
3.3 Renal system Reduction of hourly urinary output to less than 0.5ml/kg occurs early in shock, initially because of prerenal insufficiency. Without treatment,there may be rapid progression to acute tubular necrosis or cortical necrosis. Renal damage is caused by excessive sympathetic activity, circulating vasoactive substances and disseminated intravascular coagulation. 16
★ Oliguria may be profound only 2-3 ml urine hourly.If there is total anuria, an obstructive uropathy should be considered.It is important to distinguish between prerenal and renal failure because the treatment for the former is fluid repletion and for the latter is fluid restriction.In patients with cirrhosis of the liver and jaundice there is a higher incidence of acute renal failure.
17
3.4 Central nervous system There is clouding of the sensorium, confusion, agitation and eventually coma. This progression is due to hypoxia, low blood pressure, microemboli and circulating toxins.
18
3.5 Gastrointestinal system and liver 3.5.1 There may be vomiting or diarrhoea, whatever the cause of shock. Late in shock, ileus is common. Bowel sounds are infrequent or absent.The abdomen may be distended. Peritonitis is a common source of septic shock and is accompanied by abdominal pain and board-like rigidity. 19
3.5.2 Liver enlargement occurs in right ventricular failure, and jaundice can occur in the presence or absence of liver enlargement. It is common in septicemia of after massive transfusion. Hyperglycemia may occur initially in shock because of increased endogenous catecholamines. Later, however, hypoglycaemia may occur as the liver glycogen stores become depleted. 20
4. Diagnosis Step 1 look: investigating the patient’s skin and facial expression; Step 2 inquire: inquiring the history and know if his sense is clear; Step 3 touching: touching the patient’s pulse to know its intensity, speed and rhythm, and touching the temperature and humidity of the skin; Step 4 listen: listening to the heart sound and measuring the blood pressure.
21
4.1 History
There are few specific features in the history that will lead the doctor to make a diagnosis of shock, but many that should alert him to its possible impending onset.
22
4.1.1 Vomiting, diarrhoea, hematemesis and melena all may produce volume depletion sufficient to cause shock. 4.1.2 A history of peptic ulcer or chronic alcohol ingestion may precede a massive intestinal hemorrhage. 4.1.3 Trauma to chest or abdomen may lead to occult hemorrhage caused by rupture of a major vessel, liver or spleen.
23
4.1.4 Abdominal pain may be the only symptom of a ruptured viscus and consequent peritonitis. 4.1.5 Chest pain should alert the doctor to the possibility of myocardial infarction, pulmonary embolus or dissecting aorta, and their concomitant complications.
24
4.1.6 The source of bacteremic and endotoxemic shock is not always obvious. It may be iatrogenically induced. A history of predisposing factors may be available. 4.1.7 A patient in established shock cannot usually give an accurate history. Information may be obtainable only from relatives or previous medical records.
25
4.2 Investigations
The diagnosis of shock is made clinically. Investigations in shock are used to clarify the etiology, to assess the degree of organ failure, and to assess the response to therapy. These tests may be useful:Hemoglobin 、 Haematocrit 、 Urinary output 、 CVP 、 Arterial blood PH 、 PaO2 、 PaCO2 、 ECG 、 Electrolyte,et al.
26
5. Treatment The aim of therapy is to improve the supply of oxygenated blood to the tissues.
27
5.1 Restoration of optimal circulating blood volume Fluid administration is the single most important therapeutic measure in the treatment of hypovolaemia,whether it is the initial cause for shock,or a complication accounting for the progression of cardiogenic, distributive or obstructive shock.The volume and speed of administration depends on the patient’s cardiac competence and must be considered carefully if acute left ventricular failure and the resultant pulmonary edema are to be avoided. 28
5.1.1 A fluid challenge should be administered over 10min.
CVP
PCWP
fluid administered
(cmH2O)
(mmHg)
(ml)
<8 <12 200 8-14 12-16 100 ↑>5 ↑>7 stop If there is little or no response to treatment, further fluid boluses should be administered according to the guidelines given above.It is safe to maintain a CVP up to 16cmH2O and PCWP up to 18mmHg.
29
5.1.2 During massive hemorrhage, both red cells and plasma are lost,and should be replaced by whole blood. Stored blood is deficient in clotting factors; both fresh-frozen plasma and platelets may be required, depending on clotting studies.
30
5.1.3 When plasma loss is caused by inflammatory processes, e.g. peritonitis, pancreatitis or crush injury, the hemoglobin and haematocrit concentration may be raised and albumin or plasma-protein fraction should be used for the fluid challenge.
31
5.1.4 In cardiogenic shock, where the reduced intravascular volume is accompanied by a colloid osmotic pressure less than the PAWP, the fluid challenge should be with 5% human serum albumin or with a smaller volume of 20% salt-poor human albumin. Responsiveness to potent loop diuretics, such as frusemide, may be restored.
32
5.1.5 If hypovolemia is caused by fluid and electrolyte loss, infusions of normal saline with appropriate additives of potassium should be tried. Excess crystalloid transfusion in any form of hypovolemia may sufficiently reduced the plasma oncotic pressure to contribute to interstitial edema.
33
5.1.6 The use of synthetic plasma expanders is justified in primary hypovolemic shock when blood and plasma are not instantly available. Dextran increases blood viscosity and is associated with impairment of renal function and coagulation. Dextran has been the cause of hypersensitivity reactions.
34
5.2 Provision of adequate oxygenation All patients who are clinically shocked should be given supplementary oxygen. Mechanical ventilation is required if oxygenation remains inadequate, i.e. a PaO2 of less than 70mmHg or if respiratory acidosis develops, i.e. a PaCO2 of greater than 55mmHg.
35
! To prevent the risks of oxygen toxicity, the inspired oxygen concentration should be limited to 60% or less. The PaO2should be kept at about 100mmHg and PaCO2 about 40mmHg. It is better to accept lower PaO2values than to persist with inspired oxygen concentrations greater than 60%. 36
5.3 Improvement of cardiac output 5.3.1 5.3.2 5.3.3 5.3.4
Optimize preload Increase contractility Reduce afterload Correct dysrhythmias
37
5.3.1 Optimize preload The preload is optimized by restoring blood volume, as previously described.
38
5.3.2 Increase contractility
The use of drugs which increase myocardial contractility must be balanced against the cost of increased myocardial oxygen consumption if further myocardial injury is to be avoided.
39
Isoprenaline is a pureβ-stimulant.It may cause excessive tachycardia and dysrhythmias, as well as extending infarct size following coronary artery occlusion.The blood pressure may fall because of peripheral vasodilation of the voluntary muscle vessels, which also diverts blood away from renal and visceral vessels. However,the inotropic effect,accompanied by a reduction in afterload, can be beneficial in some cases.
40
Noradrenaline is predominantly an α-stimulant. It increases the tone in the postcapillary sphincter more than in the precapillary, promoting loss of fluid from the capillary beds. Noradrenaline also causes coronary vasoconstriction and decreases renal blood flow. Together with its β1 activity, its net effect is an increase in cardiac output, peripheral resistance and blood pressure.
41
Adrenaline.When used at low doses, theβeffects predomiate, with an increase in cardiac output and heart rate and reduction in peripheral resistance. At high doses,α vascular effects predominate, leading to an increased peripheral resistance and reduction in renal blood flow.
42
Dopamine,
a precursor of adrenaline, increases myocardial contractility and, to a lesser extent, heart rate, by stimulating β-adrenergic receptors.Vasodilatation occurs in the renal, mesenteric, coronary and intracerebral arterial vascular bed because of stimulation of specific dopaminergic receptors.With large doses,vasoconstriction occurs as a result of αadrenergic stimulation.
43
Dobutamine,a new synthetic cardioactive sympathomimetic amine, augments myocardial contractility without significantly increasing heart rate,and therefore increases cardiac output with less of an increase in myocardial oxyen consumption than is produced by isoprenaline.Like isoprenaline, it reduces afterload by increasing blood flow to the muscular beds.
44
Occasionally, two catecholamines appear to have a better effect when used concurrently,e.g.dopamine and isoprenaline,or dopamine and dobutamine.It must be remembered that there is a relative resistance to the action of catecholamines in the presence of acidosis,which should be corrected. 45
5.3.3 Reduce afterload
The afterload is reduced by using peripheral vasodilators. This is accompanied by a decrease in left ventricular volume and reduced left atrial and PCWP, aiding resolution of pulmonary edema.The cardiac work and oxygen demand are also decreased.
46
! Careful haemodynamic monitoring is required because excess vasodilation causes a reduction in cardiac output,a drop in arterial pressure and compromises coronary perfusion,aggravating shock.
47
5.3.4 Correct dysrhythmias Correction of dysrhythmias is important.They are often caused by electrolyte imbalance of hypoxia which should be excluded or corrected.
48
A bradycardia reduces cardiac output and can be treated with an intravenous infusion of isoprenline,with atropine,if vagally induced,or with a temporary transvenous pacing wire if the former are unsuccessful. Tachycardias of more than 140 beats/min lead to a reduction in cardiac output because of inadequate filling time for the heart. Coronary blood flow occurs during diastole,so myocardial oxygen delivery can be critically reduced when diastole is shortened by an increase in heart rate. 49
A ventricular tachycardia is particularly deleterious and must be treated by DF conversion(50-400J) or lignocaine(100mg i.v.).Maintenance may be required with a continuous lignocaine infusion or βblockers,e.g. practolol up to 20mg i.v.,at a rate of 2.5mg/min. Disopyramide(2mg/kg)is useful in treating both supraventricular and ventricular tachycardias.
50
5.4 Improvement of Cellular function 5.4.1 Glucose,potassium and insulin therapy 5.4.2 Steroid therapy
51
5.4.1 Glucose,potassium and insulin therapy Glucose,potassium and insulin therapy promotes the rapid extrusion of sodium from cells.In shock, when the function of the sodium pump is impaired by a deficiency of ATP,the cell membrane leaks, resulting in an efflux of potassium and an influx of sodium chloride and water into cells, which further impairs their function.This has been called ‘the sick cell syndrome’. 52
5.4.2 Steroid therapy Protect
the integrity of cell membranes; Stabilize lysosomal membranes, preventing the release of hydrolases; Inhibit the release of some vasoactive substances in immune reactions; Induce gluconeogenesis from amino acids and fatty acids,aiding the production of ATP; Improve tissue perfusion by dilatation of the microcirculation. 53
5.5 Provision of adequate nutrition It is very easy to forget to feed a seriously ill patient. The basal metabolic requirements are increased 20% by trauma, 50% by peritonitis and 100% by burns. Where possible, oral or nasogastric feeding should be used. If this fails, the decision to feed intravenously should be taken as soon as possible. 54
5.6 Management of complications 5.6.1 Renal failure 5.6.2 Disseminated intravascular coagulation(DIC)
55
5.6.1 Renal failure If volume replacement does not restore urinary output, diuretic therapy is tried.An intravenous infusion of hypertonic mannitol is given over 10min. If there is a response, further doses of mannitol should be given to maintain a urine output of about 100ml/h.If there is little or no response,further doses of mannitol are dangerous and may precipitate pulmonary edema or hyperosmolar syndrome.High doses of loop diuretics should be tried, e.g.frusemide 250mg. Again, if there is a response,further doses should be used to maintain a urine output.
56
If oliguria persists,the daily fluid intake should be restricted to 500ml plus any fluid losses. If the serum potassium is greater than 6.5 mmol/l a bolus of 50ml of 50% dextrose plus 8 units of soluble insulin should be given.
57
If there are cardiac dysrhythmias, 10 ml of 10% calcium gluconate should be given slowly intravenously and a metabolic acidosis should be corrected. Peritoneal or haemodialysis becomes necessary if the potassium levels cannot be lowered, if there is serious fluid overload or a gross metabolic acidosis.
58
5.6.2 Disseminated intravascular coagulation Often, correction of the cause is sufficient to return the coagulation factor to normal. However, in severe cases, heparin (5-10units/ (kg.h) by continuous infusion may be necessary until the fibrinogen degradation products disappear and fibrinogen levels return to normal (usually about 3 days).
59
Heparin enhances antithrombin activity and inhibits factors X and XI. Heparin therapy is monitored by the partial thromboplastin time. Attempts to replace coagulation factors, e.g.fibrinogen, before heparinization, may exacerbate DIC. Platelet counts may remain low, requiring a platelet transfusion.
60
5.7 Specific treatment 5.7.1 Septic shock 5.7.2 Cardiogenic shock 5.7.3 Anaphylactic shock
61
5.7.1 Septic shock If infection is suspected in a shocked patient,intravenous antibiotic therapy must be started as soon as specimens have been sent for culture,and before results are known,with the possible exception of the Gram’s stain.
62
Initial therapy for G+ organisms can be cephalothin, methicillin or vancomycin.Once the results of culture and sensitivities are known, unnecessary antibiotics should be stopped and only the appropriate therapy continued. Surgical intervention is often necessary. Operations should not be postponed because the patient is ‘too ill’,as his condition will only deteriorate unless the septic focus,such as an abscess,is drained,or is removed. 63
5.7.2 Cardiogenic shock When pharmacological agents fail in cardiogenic shock, mechanical assistance with an intra-aortic balloon pump has been used. A balloon catheter placed in the descending aorta is inflated during diastole, increasing coronary perfusion, and deflated before the opening of the aortic valve,reducing afterload.
64
5.7.3 Anaphylactic shock This is one of the few cause of shock which benefits from the administration of intravenous adrenaline and corticosteroids. An antihistamine,e.g. chlorpheniramine 10mg i.v, should also be given.
65
Conclusion The ultimate outcome in the treatment of shock depends on the reversibility of the underlying cause,the early recognition and aggressive treatment of complications.
66
THANK YOU !
67
1
1. Definition Shock is a emergency and fatal syndrome which results from poor tissue perfusion and tissue hypoxia from acute hemodynamic disturbance , leading to multiple organ dysfunction, moreover organ failure, and death. This syndrome is characterized by hypotension, pallor, cold clammy skin, alterations in mental status and reduction of urine formation. 2
2. Mechanisms A deficit in tissue perfusion can be caused by four major mechanisms: 2.1 hypovolemia; 2.2 cardiac failure; 2.3 peripheral distributive defects; 2.4 vascular obstruction.
3
2.1 hypovolemia Hypovolemia due to hemorrhage, plasma loss or extravasation of electrolytes and water results in a critical reduction of venous return to the heart, and therefore of cardiac output.
4
2.2 cardiac failure Cardiac contractility reduced by myocardial infarction,bacterial endotoxins or cardiac-depressant drugs and cardiac dysrhythmias (both tachycardias and bradycardias) ,can lead to a reduced cardiac output.
5
2.3 peripheral distributive defects Impaired peripheral distribution caused by an imbalance between precapillary sphincter and venular tone,or by the openingup of arteriolovenular communications, leads to tissue hypoxia.
6
2.4 vascular obstruction High-resistance shock is associated with intravascular sequestration of blood in the venous capacitance circuit. Any major obstruction to the circulation in the heart, major vessels or microcirculation also leads to failure to tissue perfusion.
7
3. Clinical manifestations The clinical syndrome of shock can develop over the course of a few minutes or several hours, depending on the cause; all systems may be affected.
8
3.1 Cardiovascular system Early Blood pressure Heart rate Cardiac output
N or ↓ N or ↑ N or ↑
Lately ↓ ↑ ↓
9
3.1.1 The blood pressure initially may be normal or only slightly decreased, because of compensatory vasoconstriction.Late in shock, both blood pressure and cardiac output are markedly reduced. 3.1.2 Tachycardia is usually present from the start, unless heart block is an etiological factor. 3.1.3 The peripheral pulses become thready or may be absent.
10
3.1.4 Cardiac dysrhythmias are common late in shock and are caused by hypoxia, metabolic disturbances and circulating cardiac toxins. 3.1.5 The ECG frequently shows signs of ischemia, ST depression and flattening of the T waves. 3.1.6 The CVP can initially be high in cardiogenic and obstructive shock,low in hypovolemic shock, and normal or low in bacteremic shock. 11
3.1.7 An increase in the PCWP in the presence of a low cardiac output is indicative of severe left ventricular failure. 3.1.8 The skin is a visible monitor of the state of the peripheral circulation. As shock develops, the patient becomes clammy and pale with peripheral cyanosis.The skin may feel cold,despite a high core temperature.
12
3.2 Respiratory system
Early Tachypnea Hyperpnea
Lately Tachypnea Laboured breathing Central cyanosis 13
3.2.1 Tachypnea and hyperpnea are present early in shock ， occuring in response to metabolic acidosis and hypoxemia. 3.2.2 Respiratory insufficiency has been found to be present in 62% of a series of patients with proved Gsepticaemia.
14
3.2.3 An increase in lung water leads to reduced compliance and impaired gas exchange. 3.2.4 Central cyanosis may be present. 3.2.5 The lung signs are nonspecific.On auscultation the lung may sound clear, or there may be widespread crepitations and zones of diminished air entry.
15
3.3 Renal system Reduction of hourly urinary output to less than 0.5ml/kg occurs early in shock, initially because of prerenal insufficiency. Without treatment,there may be rapid progression to acute tubular necrosis or cortical necrosis. Renal damage is caused by excessive sympathetic activity, circulating vasoactive substances and disseminated intravascular coagulation. 16
★ Oliguria may be profound only 2-3 ml urine hourly.If there is total anuria, an obstructive uropathy should be considered.It is important to distinguish between prerenal and renal failure because the treatment for the former is fluid repletion and for the latter is fluid restriction.In patients with cirrhosis of the liver and jaundice there is a higher incidence of acute renal failure.
17
3.4 Central nervous system There is clouding of the sensorium, confusion, agitation and eventually coma. This progression is due to hypoxia, low blood pressure, microemboli and circulating toxins.
18
3.5 Gastrointestinal system and liver 3.5.1 There may be vomiting or diarrhoea, whatever the cause of shock. Late in shock, ileus is common. Bowel sounds are infrequent or absent.The abdomen may be distended. Peritonitis is a common source of septic shock and is accompanied by abdominal pain and board-like rigidity. 19
3.5.2 Liver enlargement occurs in right ventricular failure, and jaundice can occur in the presence or absence of liver enlargement. It is common in septicemia of after massive transfusion. Hyperglycemia may occur initially in shock because of increased endogenous catecholamines. Later, however, hypoglycaemia may occur as the liver glycogen stores become depleted. 20
4. Diagnosis Step 1 look: investigating the patient’s skin and facial expression; Step 2 inquire: inquiring the history and know if his sense is clear; Step 3 touching: touching the patient’s pulse to know its intensity, speed and rhythm, and touching the temperature and humidity of the skin; Step 4 listen: listening to the heart sound and measuring the blood pressure.
21
4.1 History
There are few specific features in the history that will lead the doctor to make a diagnosis of shock, but many that should alert him to its possible impending onset.
22
4.1.1 Vomiting, diarrhoea, hematemesis and melena all may produce volume depletion sufficient to cause shock. 4.1.2 A history of peptic ulcer or chronic alcohol ingestion may precede a massive intestinal hemorrhage. 4.1.3 Trauma to chest or abdomen may lead to occult hemorrhage caused by rupture of a major vessel, liver or spleen.
23
4.1.4 Abdominal pain may be the only symptom of a ruptured viscus and consequent peritonitis. 4.1.5 Chest pain should alert the doctor to the possibility of myocardial infarction, pulmonary embolus or dissecting aorta, and their concomitant complications.
24
4.1.6 The source of bacteremic and endotoxemic shock is not always obvious. It may be iatrogenically induced. A history of predisposing factors may be available. 4.1.7 A patient in established shock cannot usually give an accurate history. Information may be obtainable only from relatives or previous medical records.
25
4.2 Investigations
The diagnosis of shock is made clinically. Investigations in shock are used to clarify the etiology, to assess the degree of organ failure, and to assess the response to therapy. These tests may be useful:Hemoglobin 、 Haematocrit 、 Urinary output 、 CVP 、 Arterial blood PH 、 PaO2 、 PaCO2 、 ECG 、 Electrolyte,et al.
26
5. Treatment The aim of therapy is to improve the supply of oxygenated blood to the tissues.
27
5.1 Restoration of optimal circulating blood volume Fluid administration is the single most important therapeutic measure in the treatment of hypovolaemia,whether it is the initial cause for shock,or a complication accounting for the progression of cardiogenic, distributive or obstructive shock.The volume and speed of administration depends on the patient’s cardiac competence and must be considered carefully if acute left ventricular failure and the resultant pulmonary edema are to be avoided. 28
5.1.1 A fluid challenge should be administered over 10min.
CVP
PCWP
fluid administered
(cmH2O)
(mmHg)
(ml)
<8 <12 200 8-14 12-16 100 ↑>5 ↑>7 stop If there is little or no response to treatment, further fluid boluses should be administered according to the guidelines given above.It is safe to maintain a CVP up to 16cmH2O and PCWP up to 18mmHg.
29
5.1.2 During massive hemorrhage, both red cells and plasma are lost,and should be replaced by whole blood. Stored blood is deficient in clotting factors; both fresh-frozen plasma and platelets may be required, depending on clotting studies.
30
5.1.3 When plasma loss is caused by inflammatory processes, e.g. peritonitis, pancreatitis or crush injury, the hemoglobin and haematocrit concentration may be raised and albumin or plasma-protein fraction should be used for the fluid challenge.
31
5.1.4 In cardiogenic shock, where the reduced intravascular volume is accompanied by a colloid osmotic pressure less than the PAWP, the fluid challenge should be with 5% human serum albumin or with a smaller volume of 20% salt-poor human albumin. Responsiveness to potent loop diuretics, such as frusemide, may be restored.
32
5.1.5 If hypovolemia is caused by fluid and electrolyte loss, infusions of normal saline with appropriate additives of potassium should be tried. Excess crystalloid transfusion in any form of hypovolemia may sufficiently reduced the plasma oncotic pressure to contribute to interstitial edema.
33
5.1.6 The use of synthetic plasma expanders is justified in primary hypovolemic shock when blood and plasma are not instantly available. Dextran increases blood viscosity and is associated with impairment of renal function and coagulation. Dextran has been the cause of hypersensitivity reactions.
34
5.2 Provision of adequate oxygenation All patients who are clinically shocked should be given supplementary oxygen. Mechanical ventilation is required if oxygenation remains inadequate, i.e. a PaO2 of less than 70mmHg or if respiratory acidosis develops, i.e. a PaCO2 of greater than 55mmHg.
35
! To prevent the risks of oxygen toxicity, the inspired oxygen concentration should be limited to 60% or less. The PaO2should be kept at about 100mmHg and PaCO2 about 40mmHg. It is better to accept lower PaO2values than to persist with inspired oxygen concentrations greater than 60%. 36
5.3 Improvement of cardiac output 5.3.1 5.3.2 5.3.3 5.3.4
Optimize preload Increase contractility Reduce afterload Correct dysrhythmias
37
5.3.1 Optimize preload The preload is optimized by restoring blood volume, as previously described.
38
5.3.2 Increase contractility
The use of drugs which increase myocardial contractility must be balanced against the cost of increased myocardial oxygen consumption if further myocardial injury is to be avoided.
39
Isoprenaline is a pureβ-stimulant.It may cause excessive tachycardia and dysrhythmias, as well as extending infarct size following coronary artery occlusion.The blood pressure may fall because of peripheral vasodilation of the voluntary muscle vessels, which also diverts blood away from renal and visceral vessels. However,the inotropic effect,accompanied by a reduction in afterload, can be beneficial in some cases.
40
Noradrenaline is predominantly an α-stimulant. It increases the tone in the postcapillary sphincter more than in the precapillary, promoting loss of fluid from the capillary beds. Noradrenaline also causes coronary vasoconstriction and decreases renal blood flow. Together with its β1 activity, its net effect is an increase in cardiac output, peripheral resistance and blood pressure.
41
Adrenaline.When used at low doses, theβeffects predomiate, with an increase in cardiac output and heart rate and reduction in peripheral resistance. At high doses,α vascular effects predominate, leading to an increased peripheral resistance and reduction in renal blood flow.
42
Dopamine,
a precursor of adrenaline, increases myocardial contractility and, to a lesser extent, heart rate, by stimulating β-adrenergic receptors.Vasodilatation occurs in the renal, mesenteric, coronary and intracerebral arterial vascular bed because of stimulation of specific dopaminergic receptors.With large doses,vasoconstriction occurs as a result of αadrenergic stimulation.
43
Dobutamine,a new synthetic cardioactive sympathomimetic amine, augments myocardial contractility without significantly increasing heart rate,and therefore increases cardiac output with less of an increase in myocardial oxyen consumption than is produced by isoprenaline.Like isoprenaline, it reduces afterload by increasing blood flow to the muscular beds.
44
Occasionally, two catecholamines appear to have a better effect when used concurrently,e.g.dopamine and isoprenaline,or dopamine and dobutamine.It must be remembered that there is a relative resistance to the action of catecholamines in the presence of acidosis,which should be corrected. 45
5.3.3 Reduce afterload
The afterload is reduced by using peripheral vasodilators. This is accompanied by a decrease in left ventricular volume and reduced left atrial and PCWP, aiding resolution of pulmonary edema.The cardiac work and oxygen demand are also decreased.
46
! Careful haemodynamic monitoring is required because excess vasodilation causes a reduction in cardiac output,a drop in arterial pressure and compromises coronary perfusion,aggravating shock.
47
5.3.4 Correct dysrhythmias Correction of dysrhythmias is important.They are often caused by electrolyte imbalance of hypoxia which should be excluded or corrected.
48
A bradycardia reduces cardiac output and can be treated with an intravenous infusion of isoprenline,with atropine,if vagally induced,or with a temporary transvenous pacing wire if the former are unsuccessful. Tachycardias of more than 140 beats/min lead to a reduction in cardiac output because of inadequate filling time for the heart. Coronary blood flow occurs during diastole,so myocardial oxygen delivery can be critically reduced when diastole is shortened by an increase in heart rate. 49
A ventricular tachycardia is particularly deleterious and must be treated by DF conversion(50-400J) or lignocaine(100mg i.v.).Maintenance may be required with a continuous lignocaine infusion or βblockers,e.g. practolol up to 20mg i.v.,at a rate of 2.5mg/min. Disopyramide(2mg/kg)is useful in treating both supraventricular and ventricular tachycardias.
50
5.4 Improvement of Cellular function 5.4.1 Glucose,potassium and insulin therapy 5.4.2 Steroid therapy
51
5.4.1 Glucose,potassium and insulin therapy Glucose,potassium and insulin therapy promotes the rapid extrusion of sodium from cells.In shock, when the function of the sodium pump is impaired by a deficiency of ATP,the cell membrane leaks, resulting in an efflux of potassium and an influx of sodium chloride and water into cells, which further impairs their function.This has been called ‘the sick cell syndrome’. 52
5.4.2 Steroid therapy Protect
the integrity of cell membranes; Stabilize lysosomal membranes, preventing the release of hydrolases; Inhibit the release of some vasoactive substances in immune reactions; Induce gluconeogenesis from amino acids and fatty acids,aiding the production of ATP; Improve tissue perfusion by dilatation of the microcirculation. 53
5.5 Provision of adequate nutrition It is very easy to forget to feed a seriously ill patient. The basal metabolic requirements are increased 20% by trauma, 50% by peritonitis and 100% by burns. Where possible, oral or nasogastric feeding should be used. If this fails, the decision to feed intravenously should be taken as soon as possible. 54
5.6 Management of complications 5.6.1 Renal failure 5.6.2 Disseminated intravascular coagulation(DIC)
55
5.6.1 Renal failure If volume replacement does not restore urinary output, diuretic therapy is tried.An intravenous infusion of hypertonic mannitol is given over 10min. If there is a response, further doses of mannitol should be given to maintain a urine output of about 100ml/h.If there is little or no response,further doses of mannitol are dangerous and may precipitate pulmonary edema or hyperosmolar syndrome.High doses of loop diuretics should be tried, e.g.frusemide 250mg. Again, if there is a response,further doses should be used to maintain a urine output.
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If oliguria persists,the daily fluid intake should be restricted to 500ml plus any fluid losses. If the serum potassium is greater than 6.5 mmol/l a bolus of 50ml of 50% dextrose plus 8 units of soluble insulin should be given.
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If there are cardiac dysrhythmias, 10 ml of 10% calcium gluconate should be given slowly intravenously and a metabolic acidosis should be corrected. Peritoneal or haemodialysis becomes necessary if the potassium levels cannot be lowered, if there is serious fluid overload or a gross metabolic acidosis.
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5.6.2 Disseminated intravascular coagulation Often, correction of the cause is sufficient to return the coagulation factor to normal. However, in severe cases, heparin (5-10units/ (kg.h) by continuous infusion may be necessary until the fibrinogen degradation products disappear and fibrinogen levels return to normal (usually about 3 days).
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Heparin enhances antithrombin activity and inhibits factors X and XI. Heparin therapy is monitored by the partial thromboplastin time. Attempts to replace coagulation factors, e.g.fibrinogen, before heparinization, may exacerbate DIC. Platelet counts may remain low, requiring a platelet transfusion.
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5.7 Specific treatment 5.7.1 Septic shock 5.7.2 Cardiogenic shock 5.7.3 Anaphylactic shock
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5.7.1 Septic shock If infection is suspected in a shocked patient,intravenous antibiotic therapy must be started as soon as specimens have been sent for culture,and before results are known,with the possible exception of the Gram’s stain.
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Initial therapy for G+ organisms can be cephalothin, methicillin or vancomycin.Once the results of culture and sensitivities are known, unnecessary antibiotics should be stopped and only the appropriate therapy continued. Surgical intervention is often necessary. Operations should not be postponed because the patient is ‘too ill’,as his condition will only deteriorate unless the septic focus,such as an abscess,is drained,or is removed. 63
5.7.2 Cardiogenic shock When pharmacological agents fail in cardiogenic shock, mechanical assistance with an intra-aortic balloon pump has been used. A balloon catheter placed in the descending aorta is inflated during diastole, increasing coronary perfusion, and deflated before the opening of the aortic valve,reducing afterload.
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5.7.3 Anaphylactic shock This is one of the few cause of shock which benefits from the administration of intravenous adrenaline and corticosteroids. An antihistamine,e.g. chlorpheniramine 10mg i.v, should also be given.
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Conclusion The ultimate outcome in the treatment of shock depends on the reversibility of the underlying cause,the early recognition and aggressive treatment of complications.
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