Shock

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Chapter 11 Shock

Steve Dunjey

Shock is a clinical condition, commonly encountered in practice, with multiple causes which share the final common pathway of inadequate tissue perfusion. The consequence of inadequate perfusion is that insufficient metabolic substrates (primarily oxygen) are provided to sustain cellular homeostasis. The challenge for the clinician is to manage the shock, and to simultaneously seek and treat the cause.

CAUSES AND EFFECTS

Causes of shock are loosely grouped as follows:

• hypovolaemic (inadequate circulating volume)
• cardiogenic (inadequate myocardial contractility)
• distributive (adequate volume, which is maldistributed)
• obstructive (adequate volume, with impedance of flow).

A more complete list of causes is given in Table 11.1. A patient in shock will manifest signs of:

• the cause of the shock
• inadequate tissue perfusion, with end organ dysfunction (e.g. confusion, agitation, acidosis, decreased urine output etc) (See Box 11.1.)
• compensation. The cardiovascular response predominates, and is marked by tachycardia, peripheral vasoconstriction (sweaty, pale, cold peripheries with decreased capillary return), central vasoconstriction (narrowed pulse pressure) and decreased blood flow through nonvital structures, such as abdominal viscera (manifested by decreased urine output, decreased bowel sounds). Compensation can be so effective in young patients that the underlying shock state is manifest only by tachycardia, and more fully revealed by measuring postural blood pressure drop (greater than 20 mmHg systolic). Younger patients are able to maintain an increased heart rate and cardiac output but may suddenly deteriorate when they are unable to compensate further. Elderly patients may be incapable of mounting a tachycardiac response to shock because of medications (especially beta-blockers) or underlying heart disease.

Table 11.1 Causes of shock

Type of shock Causes Signs
Hypovolaemic
Haemorrhage
Vomiting/diarrhoea
Dehydration
Addisonian crisis

Obvious external blood loss/signs of trauma/signs of concealed blood loss
Skin turgor
Dry mucous membranes
↓ JVP
Cardiogenic
Myocardial infarction (especially anterior, R ventricular)
Myocardial contusion
Acute valvular lesion
Cardiomyopathies
Arrhythmias
Extremes of pulse rate
↑ JVP
ECG evidence of AMI, arrhythmias
New murmurs
Distributive
Neurogenic/spinal cord injury
Anaphylaxis
Sepsis
Flaccid paralysis, warm peripheries, relative bradycardia, priapism
Urticaria, angioedema, wheezes
Febrile, warm peripheries, evidence of focus
Obstructive
Pulmonary embolism
Cardiac tamponade
Tension pneumothorax
Evidence of DVT, pulmonary hypertension, ↑ JVP
Distant muffled heart sounds, pulsus paradoxus, electrical alternans
Subcutaneous emphysema midline shift trachea, ↓ breath sounds

AMI, acute myocardial infarction; DVT, deep vein thrombosis; JVP, jugular venous pressure

Box 11.1 Adverse effects of shock

CNS: confusion, restlessness and decreased level of consciousness
Myocardium: may impair myocardial function in severe shock
Lung: hypoxia, and sustained shock may induce adult respiratory distress syndrome in survivors
Liver: elevation of hepatic transaminases and bilirubin
Gastrointestinal tract: ischaemia, ileus, diarrhoea, stress ulceration and bacterial translocation into the systemic circulation
Kidney: oliguria and renal failure
Coagulopathy
Other tissue damage: all tissues are impaired by sustained underperfusion, but the processes involved are difficult to quantify

OVERVIEW OF MANAGEMENT

Shocked patients should be managed in a fully monitored area. The assessment and treatment of the shocked patient should occur in parallel. Initial treatment focuses on resuscitation, monitoring (to assess response to treatment) and seeking a specific cause (history, examination and investigations). Once the cause of shock has been determined, specific therapy should be considered. What follows is a description of initial management, then a description of specific therapies once the cause is known.

Airway and breathing

1. Secure the airway.
2. Enhance oxygenation. All patients will benefit from supplemental oxygen: initially provide the highest level of inspired O2 available.
3. Support ventilation if necessary.

Circulation

1. Control accessible haemorrhage.
2. Gain intravenous access with a minimum of two large-bore peripheral IV lines.
3. Begin fluid replacement. The volume of fluid replacement required will depend to a great degree on the type of shock being treated. Hypovolaemic shock commonly requires large volumes of fluid replacement, whereas patients with cardiogenic shock may require very little, if any at all. It is reasonable to begin with 300–500 mL boluses of fluid, and to review the response.
4. If the patient demonstrates ongoing signs of shock despite adequate volume replacement, the use of inotropic/vasopressor support should be considered.

Monitoring

Monitoring may include pulse rate, non-invasive blood pressure, urine output, temperature, central venous pressure (CVP), pulse oximetry and ECG. If the blood pressure remains low, or the patient is perceived to be unstable, invasive arterial monitoring should be considered.

Investigations

The cause of shock should be sought, and investigations appropriate to make a diagnosis should be performed on the basis of the history and exam findings. In general terms, patients will often have baseline blood tests performed (FBC, electrolytes, group and hold or crossmatch if blood loss is the likely cause, coagulation profile), ECG and CXR.

HYPOVOLAEMIC SHOCK

Hypovolaemic shock involves the loss of intravascular volume. Among the most common causes in patients presenting to the emergency department are blood loss (external, internal) and dehydration. The aims of management are to limit further fluid loss and replenish circulating intravascular volume. External haemorrhage is best controlled with direct pressure. Currently the use of military antishock trousers (MAST) is controversial and appears limited to patients with major pelvic and lower limb injuries where the device stabilises fractures and produces pelvic compression, which limits further blood loss. Adequacy of fluid resuscitation can be judged by the response of measured cardiovascular parameters (pulse rate, blood pressure, central venous pressure, urine output). Fluids used include crystalloids and colloids, although currently crystalloids are used more frequently.

Management

1. Assess and treat airway, breathing and circulation (ABCs).
2. The initial fluid of choice is usually an isotonic crystalloid (normal saline/Hartmann’s), which is probably best delivered as 300–500 mL aliquots rapidly infused (or 20 mL/kg aliquots for children).
3. Consider the use of blood products if blood loss is the primary cause of shock. If necessary (e.g. in established shock, with ongoing loss of blood) transfuse O-negative blood until either group-specific or fully crossmatched blood is available.
4. Large-bore peripheral lines are preferred. Central venous catheters (CVCs) can be time consuming, difficult to perform, and have the potential to cause injury. CVCs can be used if peripheral access proves impossible, or at a later stage when resuscitation is well established. Intraosseous access is an important alternate route in the shocked paediatric patient, and should be attempted if normal peripheral access is difficult or impossible.
5. Surgically correctible sources of blood loss should be sought, and haemorrhage arrested. Some sources of haemorrhage may be controlled medically (e.g. oesophageal varices with infusion of IV octreotide)
6. The end point of fluid therapy is still the subject of debate. Normal parameters may be detrimental in patients with some conditions which require surgical control of a bleeding source (examples include ruptured abdominal aneurysm, ectopic pregnancy, truncal stab wounds). Inadequate fluid resuscitation is, however, still a cause of preventable death, particularly in younger shocked patients, and the aim of therapy in most patients is return of near normal blood pressure. A sustained low pressure in bleeding patients is known to produce the triad of hypothermia, acidosis and coagulopathy.
7. Ongoing blood loss may produce coagulopathy, requiring treatment with appropriate doses of cryoprecipitate, fresh frozen plasma etc.

CARDIOGENIC SHOCK

Cardiogenic shock results from cardiac dysfunction with decreased cardiac output. With increasing ventricular dysfunction, florid pulmonary oedema may develop. There are often prominent signs of right ventricular failure, such as jugular venous distension (JVT).

The most common initiating event for cardiogenic shock is acute ischaemic damage to the myocardium. Once more than 40% of the myocardium is affected, ejection fraction falls, and cardiogenic shock results from the reduced cardiac output. Ischaemia can also trigger cardiogenic shock by producing papillary muscle dysfunction, septal defects, free-wall rupture or right ventricular infarction. Traditionally, tachy- and bradyarrythmias are listed separately although both can cause shock.

Cardiogenic shock is a highly lethal condition with a mortality rate in excess of 80% if a non-invasive, supportive approach is used. Preventing cardiogenic shock from developing is the most effective therapy, and every effort should be made to limit infarct size in patients with acute myocardial infarction (AMI). It seems clear that percutaneous transluminal coronary angioplasty (PTCA) or emergency coronary artery bypass is more effective than thrombolytic therapy.

Management

1. Assess and treat ABCs.
2. Maintaining an adequate blood pressure can be difficult, particularly because the volumes of fluid used in normal resuscitation can have an adverse effect, causing further dilatation of the compromised ventricle. The patient’s condition does not always allow time for institution of sophisticated monitoring (e.g. Swan–Ganz catheter) and may force the clinician to administer empiric therapy. If the patient is already in pulmonary oedema, a fluid bolus should be avoided, but for other patients it is acceptable to try incremental small boluses of crystalloid as a first step (100–250 mL).
3. If there is no response to a fluid challenge, a vasopressor is required. Commonly used agents include dobutamine and dopamine.
4. Afterload reduction leads to improved cardiac function, but further reduction in blood pressure may compromise the function of other vital organs. Afterload reduction is therefore something to institute with caution to prevent exacerbation of hypotension.
5. Specific therapy includes aspirin, control of arrhythmias and reperfusion of the infarcted area.
6. Consider the use of intra-aortic balloon pump for patients who remain haemodynamically unstable.

DISTRIBUTIVE SHOCK

A number of pathological conditions cause distributive shock, the hallmarks of which are maldistribution of intravascular fluid through microvascular leak and/or vasodilation.

Septic shock

(See also ‘Sepsis’ in Chapter 41, ‘Infectious diseases’.)

Septic shock results from a host response to infection with triggering of an immunologic cascade. While the microbiological products are harmful, the widespread and unregulated host response produces chemical mediators which harm the host as well as the infecting organism. Chemical mediators involved include the complement system, leukotrienes, prostaglandins, thromboxanes, histamine, bradykinins, tumour necrosis factor (TNF) and interleukin-1.

Septic shock occurs in approximately 50% of those with gram-negative bacteraemia, and in about 20% of those with Staphylococcus aureus bacteraemia. The gram-negative organisms most often implicated are E. coli, Klebsiella, Pseudomonas, Enterobacter and Proteus species.

Septic shock is marked clinically by signs of infection (although this may not be obvious in the immunocompromised or those at extremes of age) and vasodilation (warm peripheries despite hypotension). Eventually, myocardial dysfunction adds to the instability caused by microvascular leak and vasodilation.

Recent publications by Rivers et al (see ‘Recommended reading’) have led to the widespread acceptance of early goal-directed therapy.

Management

1. Assess and treat ABCs.
2. Large volumes of IV fluid may be required.
3. In addition to fluids, inotropes are likely to be necessary, and should be chosen to address the twin problems of decreased systemic vascular resistance as well as decreased myocardial function. Noradrenaline is an appropriate agent.
4. Sophisticated, invasive monitoring is usually required, including an arterial blood pressure monitor and central pressure monitoring. Current thinking is that better outcomes are reached with early goal-directed therapy, which follows set guidelines for physiological parameters, including central venous pressure (CVP) 8–12 mmHg, mean arterial pressure (MAP) > 65 mmHg, central venous oxygen saturation (SvO2) > 70%, urine output > 0.5 mL/kg/h.
5. The source of sepsis should be aggressively and rapidly sought. It is appropriate to administer empiric antibiotic therapy, unless a focus can be established. Other treatments may include surgical drainage, debridement or laparotomy.

Anaphylactic shock

(See also anaphylaxis flow chart, Figure 40.1.)

Anaphylactic shock results from the release of chemical mediators from mast cells and basophils. These chemicals (including histamine, leukotrienes, tumour necrosis factor, various cytokines, etc) cause vasodilation and capillary leakage, and subsequently hypotension. In addition, they can cause life-threatening compromise of the upper airway (angio-oedema) and ventilation (bronchospasm).

Clinically the syndrome is marked by a recent exposure to an allergen, the presence of urticaria/angio-oedema (90% of patients), bronchospasm, rhinitis, conjunctivitis and gastrointestinal cramping.

Recently, published work by Brown et al (see ‘Recommended reading’) has led to a re-emphasis on the use of adrenaline, and recommendations against the use of ancillary medications.

Management

1. Place the patient in the supine position (or left lateral position for vomiting patients).
2. Give IM adrenaline 1:1000, at a dose of 0.01 mg/kg body weight to a maximum dose of 0.5 mg (0.5 mL), injected into the lateral thigh.
3. All patients will benefit from supplemental oxygen and IV fluids. Use normal saline.
4. Support airway and ventilation. Be ready to deal with rapid progressive loss of airway. Be ready for resistant bronchospasm.
5. Remove the offending agent if possible.
6. Re-examine the patient frequently to assess progress. If resuscitation with IM adrenaline and IV normal saline is not effective, an infusion of IV adrenaline may be required: 1 mg of adrenaline added to 100 mL of normal saline can be run at 30–100 mL/h (5–15 μg/min).
7. Medications such as corticosteroids, antihistamines (H1 and H2) and antileukotrienes have no proven impact on the dangerous effects of anaphylaxis. They may have some benefit in treating mild allergic reactions involving skin. Promethazine can make vasodilation and hypotension worse.

Neurogenic shock

Neurogenic shock occurs when sympathetic tone is lost following spinal cord transection above the T6 level (T4–T8). Loss of sympathetic tone causes peripheral vasodilation and is classically associated with bradycardia.

Management

1. Assess and treat ABCs. If the level of injury is high enough (e.g. high cervical) there may be compromised ventilatory effort.
2. Engage in a thorough search for other causes of hypotension. Blood loss should be sought and confidently excluded before hypotension is attributed to neurogenic causes alone.
3. If neurogenic shock does need to be treated, it is relatively unresponsive to fluid resuscitation, and overhydration is to be discouraged. Patients may require treatment with inotropic/vasopressor agents to effectively raise blood pressure.

OBSTRUCTIVE SHOCK

Obstructive shock is hypotension due to impeded venous return. Circulatory volume is normal, but blood flow through the heart is compromised.

Specific clinical signs are of impeded venous return (distended neck veins) and also of the cause.

Pericardial tamponade

Pericardial tamponade occurs when fluid accumulates in the pericardial space, compressing the heart and eventually impairing cardiac filling. Classically, patients manifest Beck’s triad (hypotension, elevated JVP, and muffled heart sounds), and may have marked pulsus paradoxus. Clinical deterioration can be rapid. ECG may show electrical alternans, and the diagnosis can be established definitively with echocardiography.

Management

1. Assess and treat ABCs.
2. All patients benefit from IV fluids and oxygen.
3. Specific therapy is emergent pericardiocentesis (which ideally should be done with echo and ECG guidance) or open thoracotomy.
4. Other specific therapies depend on the cause of the effusion.

Tension pneumothorax

Obstructive shock results from a tension pneumothorax when raised intrathoracic pressure induces collapse of cardiac chambers and subsequent impaired cardiac filling. Specific signs include respiratory distress, with shift of the trachea from the midline and a hyperresonant, quiet chest on the side of the pneumothorax. The diagnosis is clinical, and should not depend on a confirmatory chest X-ray.

Management

1. Assess and treat ABCs.
2. Specific therapy is to drain the pneumothorax, initially by needle thoracostomy, immediately followed by a formal intercostal catheter.
3. Sucking chest wounds can cause a tension pneumothorax and should be covered with a non-permeable dressing stuck down on three sides, in addition to draining the pneumothorax.
4. A pneumothorax that resists drainage and continues to bubble vigorously may represent an injury to a major airway. Cardiothoracic help should be sought.

Pulmonary embolism

Massive pulmonary embolism can cause obstructive shock (see chapter 10, ‘Pulmonary emboli and venous thromboses’).

SUMMARY

There are many causes of shock, but the initial approach is always the same. Secure an airway, supplement ventilation if necessary, provide oxygen and resuscitate with IV fluids (except for cardiogenic shock). The cause of the shock should be sought, and specifically treated as appropriate.

RECOMMENDED READING

Annane D., Sebille V., Charpentier C., et al. Effect of treatment with low doses of hydrocortisone and fludricortisone on mortality in patients with septic shock. JAMA. 2002;288(7):862-871.

Brown S.G., Mullins R.J., Gold M.S. Anaphylaxis: diagnosis and management. Med J Aust. 2006;185(5):283-289.

Burris D., Rhee P., Kaufmann C., et al. Controlled resuscitation for uncontrolled haemorrhagic shock. The Journal of Trauma. 1999;46(2):216-222.

Dutton R., Mackenzie C., Scalea T. Hypotensive resuscitation during active haemorrhage: impact on in-hospital mortality. The Journal of Trauma. 2002;52(6):1141-1146.

McCunn M., Karlin A. Nonblood fluid resuscitation. Anaesthesiology Clinics of North America. 1999;17(1):107-121.

McGee S., Abernethy W., Simel D. Is this patient hypovolaemic? JAMA. 1999;281(11):1022-1029.

Rivers E., Nguyen B., Havstad S., et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368-1377.

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