BMJ Learning

Shock: a guide to diagnosis and management

د. حسين محمد جمعة
اختصاصي الامراض الباطنة
البورد العربي
كلية طب الموصل
2010

Key points

Shock is an important cause of morbidity and mortality
If not promptly recognised and reversed, shock leads to progressive cellular injury, multiple organ failure, and death
Classic clinical signs such as hypotension and oliguria often occur late and their absence does not exclude the diagnosis of shock
You should treat patients with shock in a critical care environment.

What is shock and why is it important?

Shock is a clinical state with diverse causes that occurs as a consequence of inadequate tissue perfusion, leading to an insufficient oxygen supply for the patient's metabolic requirements. This imbalance results in tissue hypoxia and lactic acidosis, which, if not promptly reversed, leads to progressive cellular injury, multiple organ failure, and death.
Shock is an important cause of morbidity, accounting for 34% of admissions to the intensive care unit, with mortality rates of 50-60% for septic shock and 60-80% for cardiogenic shock.


The pathophysiology of shock: global oxygen delivery and tissue oxygenation
Global indices of tissue oxygenation
To manage shock correctly you need to understand the principles of oxygen delivery and oxygen consumption. In an individual patient, the total amount of oxygen delivered to the tissues is the product of cardiac output and the arterial oxygen content. The arterial oxygen content depends on:
• Arterial oxygen saturation
• Haemoglobin levels
• The amount of oxygen dissolved in the plasma.

Normally, only 20-30% of the delivered oxygen is extracted by the tissues (oxygen extraction ratio). The remaining oxygen returns to the venous circulation and can be measured using a central venous catheter (central venous oxygen saturation) or in the pulmonary artery using a pulmonary artery catheter (mixed venous oxygen saturation).

Generally, shock is associated with a fall in oxygen delivery secondary to

• a reduction in cardiac output,
• arterial oxygen saturation, or
• haemoglobin levels.
To meet their oxygen requirements and maintain a constant oxygen consumption, the tissues adapt to the lower levels of oxygen delivered to the tissues by extracting a larger fraction of the delivered oxygen.

Tissues, however, cannot extract more than 60% of the oxygen delivered. Therefore, if oxygen delivery falls below a critical value, tissue hypoxia will result in a low mixed venous oxygen saturation (<65%) or central venous oxygen saturation (<70%) and anaerobic metabolism with increased lactate concentration.

Classification

The development of shock is related to the alteration of one or more of the four main components that regulate cardiovascular performance:
Circulating blood volume
Heart rate, rhythm, and contractility
Arteriolar tone, which regulates the arterial blood pressure and tissue perfusion
Tone of the venous capacitance system, which regulates the venous return to the heart and the ventricular preload.


Shock can be classified into three categories based on the cause.
1. Hypovolaemic shock
Hypovolaemia is the most common cause of shock. Inadequate circulating volume results from:
• Blood loss (trauma or gastrointestinal bleeding)
• Fluid loss (diarrhoea or burns)
• Sequestration of fluid in the third space (obstruction of the bowel or pancreatitis).

In patients with hypovolaemia, decreased intravascular volume leads to a reduction in the venous return, stroke volume, and, ultimately, cardiac output and oxygen delivery.
Patients can compensate for a reduction of up to 25% of the circulating volume by increasing endogenous catecholamines that cause vasoconstriction of the venous capacitance system and increase venous return. During this compensatory period, patients may display signs of peripheral vasoconstriction and a low output state with cool, clammy, mottled skin, tachycardia, and poor capillary refill.

2. Cardiogenic shock

a state of inadequate tissue perfusion due to dysfunction of the myocardial pump. You can usually diagnose it by the presence of:
A systolic blood pressure of <90 mm Hg or a mean arterial pressure (MAP) <65 mm Hg for more than one hour that is not responsive to fluid administration
A cardiac index <2.2 l/min/m2
An elevated end diastolic filling pressure (pulmonary artery occlusion pressure >18 mm Hg) and pulmonary oedema.
But the absence of pulmonary congestion and hypotension at initial clinical evaluation does not exclude a diagnosis of cardiogenic shock.
There are many different causes of cardiogenic shock. These can be divided into four categories (Table 1).

Table 1: Causes of cardiogenic shock

Categories
Causes
Myocardial diseases
Myocardial infarction or ischaemia
Cardiomyopathies
Myocarditis
Arrhythmias
Ventricular more commonly than supraventricular
Valvular diseases
Acute aortic regurgitation
Critical aortic stenosis
Mitral regurgitation caused by rupture of a papillary muscle or chordae tendineae
Ventricular septal defects
Obstructive
Pulmonary embolism
Tension pneumothorax
Constrictive pericarditis
Pericardial tamponade


The most frequent cause of cardiogenic shock is acute myocardial infarction. Cardiogenic shock occurs in about:
5-15% of patients with ST elevation myocardial infarction at presentation
2.5% of patients with non-ST elevation myocardial infarction.
Patients who present with cardiogenic shock have a higher in-hospital mortality rate than those who develop cardiogenic shock later in their admission (75% versus 56%), but have a similar response to emergency revascularisation.

Although initial reports of cardiogenic shock were in patients with large infarctions associated with the loss of more than 40% of the left ventricle and more severe coronary artery disease, cardiogenic shock can also occur in patients with a non-ST elevation acute coronary syndrome.
Ischaemia can also cause diastolic heart failure with elevated end diastolic pressures and low stroke volume but a normal ejection fraction. Therefore, cardiac failure cannot always be excluded in the presence of a normal left ventricular ejection fraction.

3. Vasodilatory shock

the tissue hypoxia is caused by an ineffective tissue oxygen extraction and the loss of vasoregulatory control leading to inappropriate vasodilatation and maldistribution of blood flow. Cardiac output is typically preserved or increased.
Causes of vasodilatory shock include:
• Severe sepsis (accounting for about 3% of hospital admissions and 15% of admissions to intensive care)
• Neurogenic shock after cerebral or spinal cord injury, leading to loss of vasomotor tone and bradycardia
• Anaphylaxis
• Drug reactions
• Adrenal failure
• And rarely conditions associated with the formation of peripheral shunts, such as chronic liver failure and Paget's disease.

Clinical assessment of shock

The clinical manifestations of shock largely depend on the cause, but there are several clinical features that are common and should be promptly recognised:
Cool, clammy, with weak pulses (hypodynamic) or warm, dilated peripheries with bounding pulses (hyperdynamic)
Altered mental status
Oliguria
Hypotension or postural fall in blood pressure
Metabolic acidosis.


Oliguria (urine output <0.5 ml/kg/h) may reflect reduced renal blood flow in hypodynamic shock and is an objective measure of intravascular volume depletion and cardiac output.
But the impact of sepsis on renal blood flow in humans is more complex and largely unknown. In experimental sepsis, renal blood flow is decreased in 62% of patients and unchanged or increased in 38% of patients.

It seems that cardiac output has a dominant effect on renal blood flow during sepsis, such that in the presence of a decreased cardiac output renal blood flow is typically decreased, whereas in the presence of a preserved or increased cardiac output renal blood flow is typically maintained or increased. Nevertheless, the renal perfusion pressure is generally decreased as a result of renal vasodilatation.

The presence of oliguria and acute renal failure is strongly associated with in-hospital mortality. Hypotension (systolic blood pressure <90 mm Hg or mean arterial pressure <65 mm Hg) occurs in most patients with shock. However, in the early phases of shock hypotension may only be relative to the patient's baseline blood pressure. As a result, a drop in systolic blood pressure greater than 40 mm Hg suggests impending shock. During the later stages, profound hypotension may occur and vasopressors are often necessary to maintain adequate perfusion pressure.

You can assess the presence of metabolic acidosis by analysing arterial blood gas. This reflects poor peripheral perfusion and increased lactate production due to anaerobic metabolism.

Table 2: Investigations in shock

Initial investigations
Full blood count
Clotting studies
Renal and liver function tests
Glucose levels
Blood cultures, taken before administering antibiotics
Culture of sputum, urine, wound, or any other possible source of infection
Troponin levels
Arterial blood gases, including lactate
Electrocardiogram
Chest x ray
• Initial investigations in shock
• The initial assessment of patients with shock is aimed at identifying the underlying cause and the presence and severity of tissue hypoperfusion. More specific investigations are required to confirm the likely cause (Table 2).
Initial investigations in shock
The initial assessment of patients with shock is aimed at identifying the underlying cause and the presence and severity of tissue hypoperfusion. More specific investigations are required to confirm the likely cause (Table 2).


Further investigations
Echocardiogram in patients with cardiogenic or obstructive shock
Coronary angiogram in patients with acute coronary syndromes
Computed tomography pulmonary angiogram for patients with a suspected pulmonary embolism
Endoscopy for patients with suspected haemorrhage
Amylase levels for patients with suspected pancreatitis

How should you monitor patients with shock?

You should monitor patients with shock in a critical care environment. They will need continuous monitoring of:
• Blood oxygen saturation (with pulse oximetry)
• Blood pressure
• Respiratory rate
• Core body temperature
• Electrocardiography.

In addition, many patients will need more invasive monitoring. This will include:

A urinary catheter to monitor urine output hourly
Intra-arterial monitoring to obtain arterial blood samples for gases, acid-base balance, and arterial lactate, and to monitor blood pressure and titrate vasoactive drugs
A central venous catheter for administrating fluids and vasoactive drugs and measuring the central venous pressure (CVP).
Although the central venous pressure may help to identify hypovolaemia when it is low (<5-8 mm Hg), it does not help to guide fluid management when it is higher than 12 mm Hg. This is because the relationship between central venous pressure and ventricular preload volume is not predictable and linear, but reflects the compliance of the cardiovascular and respiratory systems


A pulmonary artery catheter - this is rarely needed for diagnosing and managing patients with shock and its clinical usefulness and safety in critically ill patients has been questioned in recent studies.

Several other less invasive devices are capable of continuously monitoring cardiac output and ventricular preload. The most commonly employed are:
Calibrated systems
PiCCOplus system (Pusion, Munich, Germany: which employs transpulmonary thermodilution) for the calibration of the continuous cardiac output algorithm
LidCO plus system (LidCO plus, London, UK; which utilises transpulmonary lithium dilution) to calibrate the continuous CO algorithm.
These systems can calculate cardiac output and volumetric indices of preload to assess the patient's fluid status.

Uncalibrated systems

LidCO Rapid (LidCO, London, UK)
FloTrac/Vigileo; (Edwards Lifesciences, Irvine, CA, USA)
MostCare/Pressure Recording Analytic Method (PRAM) (Vytech Health, Padova, Italy)
Oesophageal Doppler
All these systems have advantages and disadvantages. The use of oesophageal Doppler as a continuous monitor is limited in critically ill patients because the cardiac output measurement is crucially dependent on the positioning of the probe, which can be displaced and is difficult to use in awake patients.

How to assess global tissue oxygenation

Measuring three easily obtainable parameters can indirectly assess global tissue oxygenation and perfusion in patients with shock:
• Mixed or central venous oxygenation
• Arterial blood lactate
• Difference between mixed venous and arterial pCO2.
All these values are blood flow weighted averages of all organs and must therefore be considered as total body measurements (they do not exclude hypoxia at the single organ level).


Mixed and central venous oxygenation
Mixed venous oxygenation represents the amount of oxygen in systemic circulation that is left after passage through the tissues. It is probably the best indicator of the balance between oxygen delivery and consumption and is therefore an indicator of the degree of oxygen extraction.

pH and blood lactate

Metabolic acidosis and raised lactate levels are common markers of tissue hypoxia. Plasma lactate has been shown to have prognostic value in critically ill patients, and can be followed sequentially to assess the response to therapy. You should measure arterial lactate levels in all patients with suspected shock or severe sepsis. Although lactate levels have been considered a marker of tissue perfusion, increased lactate levels can also result from:
Sepsis mediated cellular mitochondrial dysfunction with altered efficiency to utilise oxygen
Increased production consequent to stimulation of catecholamines
Reduced liver clearance.

Difference between the venous and arterial pCO2

The difference between the venous and arterial pCO2 is measured as the difference between contemporaneous measurements of central venous or mixed pCO2 and the arterial pCO2. It reflects the adequacy of venous blood flow to remove the tissue CO2, and therefore is an expression of cardiac output.

Managing patients with shock

Shock is a medical emergency that requires prompt recognition and early, targeted interventions. The initial management of shock comprises general measures common to all types of shock, and specific interventions that vary according to the specific cause.
The goals of initial resuscitation are:
Mean arterial pressure >65 mm Hg
Central venous pressure 8-12 mm Hg
Urine output >0.5 ml/kg/h
Central venous oxygen saturation >70% (or a mixed venous oxygen saturation >65%)
Haematocrit 30%.


General measures
Oxygen
All shocked patients should receive high flow oxygen, delivered via a facemask. Continuous positive airway pressure may be required for more severe hypoxia, laboured breathing, or in patients with pulmonary oedema. The goal should be to maintain the PaO2 >8 kPa and to reduce the work of breathing, in order to decrease oxygen consumption by the respiratory muscles. In a proportion of patients with shock, respiratory muscle fatigue and acidosis demand early intubation and mechanical ventilation.

Fluid therapy: what fluid and how much?

Hypovolaemia is present in most patients with any type of shock. Therefore, the first goal of early resuscitation is to restore the intravascular volume (to increase cardiac output and oxygen delivery).
The choice of replacement fluid depends in part on the type of fluid that has been lost. Both crystalloids (isotonic saline or lactate Ringer's solution) and colloids may be used for fluid resuscitation.

Although normal saline is most frequently used, our preference is for compound sodium lactate (Hartmann's solution), which is less likely to cause hyperchloraemic acidosis, renal dysfunction, or to interfere with the assessment of acid-base balance. But the adequacy of fluid resuscitation seems more important than the type of fluid given.

Although there is no evidence to support recommendation of one type of fluid over another, colloids have the advantage of producing faster and greater intravascular volume expansion than crystalloids. Therefore, colloids are often used as first line agents for a fluid challenge, followed by crystalloids. The SAFE (Saline versus Albumin Fluid Evaluation) trial showed no difference in 28 day mortality between the two groups, although post hoc analysis suggested that in septic shock there may be a potential survival benefit with the use of 4% albumin.

A fluid challenge should be given as a rapid bolus of 500-1000 ml of crystalloids or 300-500 ml of colloids over 30 minutes, repeated up to an initial resuscitation volume of 20-40 ml/kg body weight of crystalloids and 0.2-0.3 g/kg of colloids (corresponding to ~5 ml/kg for the most commonly used colloids). Fluid resuscitation should be closely monitored so that the response to therapy can be assessed in terms of changes in blood pressure or stroke volume, to achieve a central venous pressure >8-12 mm Hg, or to detect worsening of oxygenation and pulmonary oedema.

Some patients initially show a poor response to fluid and assessment of the intravascular volume status and fluid responsiveness can be performed using more invasive haemodynamic monitoring. However, considering that the clinical endpoint of fluid resuscitation is the increase in cardiac output, stroke volume, or blood pressure, these parameters may be more useful than the preload indices.

Beware that while early, aggressive fluid therapy is appropriate in severe sepsis and septic shock, fluids may be harmful when the circulation is no longer fluid responsive and beyond the resuscitation period. The liberal use of fluids and positive fluid balances are associated with a higher morbidity and mortality.

You should consider a blood transfusion in the following circumstances.

1. During the resuscitation phase
In the presence of a low central venous oxygen saturation and a haematocrit <30%.
A haematocrit >35% is not necessary for adequate oxygen transport and may increase blood viscosity, potentially leading to stasis in the already compromised capillary circulation.
2. After the resuscitation phase
If the haemoglobin level is <7.0 g/dl in the absence of coronary artery diseases (target: 7-9 g/dl).
In the presence of coronary artery disease a higher target may be desirable (9-10 g/dl).


Inotropic and vasoactive drugs
The initial choice of vasoactive drug depends on the cause of the shock and on haemodynamic parameters such as the mean arterial pressure and cardiac output.
Vasoactive drugs should:
Optimise mean arterial pressure
Maintain diastolic pressure (this is important for coronary perfusion)
Increase stroke volume
Avoid tachycardia (to maintain an adequate ventricular diastolic filling time - this is also important for coronary perfusion).

The most frequently used vasopressor is norepinephrine (80.2% of patients), either alone or in combination. Dopamine is commonly used in Europe, although <5% of patients received dopamine in the UK.
vasopressin: In patients with refractory shock (presence of shock despite adequate fluid resuscitation and high dose norepinephrine/dopamine), vasopressin (0.03 units/min) can be considered. Higher doses (0.067 units/min) have been suggested to be beneficial in more severe shock, however, with no data on mortality benefit.

A recent trial showed the use of dopamine was associated with a greater number of adverse events and increased mortality in the subgroup of patients with cardiogenic shock. Phenylephrine may be useful when tachycardia or arrhythmias preclude the use of agents with beta-adrenergic activity.

Dopamine is a natural catecholamine formed by the decarboxylation of 3,4-dihydroxyphenylalanine (DOPA). It is a precursor to norepinephrine in noradrenergic nerves and is also a neurotransmitter in certain areas of the CNS especially in the nigrostriatal tract, and in a few peripheral sympathetic nerves. It is released from the hypothalamus and aids with bodily functions such as movement, cognitive functions, motivation and pleasure.

Dopamine produces positive chronotropic and inotropic effects.

This is accomplished directly by exerting an agonist action on beta-adrenoceptors and indirectly by causing release of norepinephrine from storage sites in sympathetic nerve endings.

The predominant effects of dopamine are dose-related, although actual response of an individual patient will largely depend on the clinical status of the patient at the time the drug is administered. At low rates of infusion (0.5-2 mcg/kg/min) dopamine causes vasodilation that is presumed to be due to a specific agonist action on dopamine receptors (distinct from alpha and beta adrenoceptors) in the renal, mesenteric, coronary, and intracerebral vascular beds. At these dopamine receptors, haloperidol is an antagonist. The vasodilation in these vascular beds is accompanied by increased glomerular filtration rate, renal blood flow, sodium excretion, and urine flow. Hypotension sometimes occurs. An increase in urinary output produced by dopamine is usually not associated with a decrease in osmolarity of the urine.

At intermediate rates of infusion (2-10 mcg/kg/min) dopamine acts to stimulate the beta1-adrenoceptors, resulting in improved myocardial contractility, increased SA rate and enhanced impulse conduction in the heart. There is little, if any, stimulation of the beta2-adrenoceptors (peripheral vasodilation). Dopamine causes less increase in myocardial oxygen consumption than isoproterenol, and its use is not usually associated with a tachyarrhythmia. Clinical studies indicate that it usually increases systolic and pulse pressure with either no effect or a slight increase in diastolic pressure. Blood flow to the peripheral vascular beds may decrease while mesenteric flow increases due to increased cardiac out put . At low and intermediate doses, total peripheral resistance (which would be raised by alpha activity) is usually unchanged.


At higher rates of infusion (10-20 mcg/kg/min) there is some effect on alpha-adrenoceptors, with consequent vasoconstrictor effects and a rise in blood pressure. The vasoconstrictor effects are first seen in the skeletal muscle vascular beds, but with increasing doses they are also evident in the renal and mesenteric vessels.
At very high rates of infusion (above 20 mcg/kg/min), stimulation of alpha-adrenoceptors predominates and vasoconstriction may compromise the circulation of the limbs and override the dopaminergic effects of dopamine, reversing renaldilation and natriuresis

Suggested Dilution: Transfer contents of one or more ampuls or vials by aseptic technique to either 250 mL or 500 mL of one of the following sterile intravenous solutions:
Sodium Chloride Injection, USP
Dextrose (5%) Injection, USP
Dextrose (5%) and Sodium Chloride (0.9%) Injection, USP
5% Dextrose in 0.45% Sodium Chloride Solution
Dextrose (5%) in Lactated Ringer's Solution
Sodium Lactate (1/6 Molar) Injection, USP
Lactated Ringer's Injection, USP
DOPAMINE has been found to be stable for a minimum of 24 hours after dilution in the sterile intravenous solutions listed above. However, as with all intravenous admixtures, dilution should be made just prior to administration.
Do NOT add DOPAMINE Injection to Sodium Bicarbonate or other alkaline intravenous solutions, since the drug is inactivated in alkaline solution.

Dopamine's onset of action occurs within five minutes of intravenous administration, and with dopamine's plasma half-life of about two minutes, the duration of action is less than ten minutes. If monoamine oxidase (MAO) inhibitors are present, however, the duration may increase to one hour. The drug is widely distributed in the body but does not cross the blood-brain barrier to a significant extent. Dopamine is metabolized in the liver,kidney, and plasma by MAO and catechol-O-methyltransferase to the inactive compounds homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid.

About 25% of the dose is taken up into specialized neurosecretory vesicles (the adrenergic nerve terminals), where it is hydroxylated to form norepinephrine. It has been reported that about 80% of the drug is excreted in the urine within 24 hours, primarily as HVA and its sulfate and glucuronide conjugates and as 3,4-dihydroxyphenylacetic acid. A very small portion is excreted unchanged.

Dobutamine is considered a direct

beta1-adrenergic agonist. It also has mild beta2- and alpha1-adrenergic effects at therapeutic doses. These effects tend to balance one another and cause little direct effect on the systemic vasculature. In contrast to dopamine, dobutamine does not cause the release of norepinephrine. It has relatively mild chronotropic, arrhythmogenic, and vasodilative effects.



Increased myocardial contractility and stroke volumes result in increased cardiac output. Decreases in left ventricular filling pressures (wedge pressures) and total peripheral resis­tance occur in patients with a failing heart. Blood pressure and cardiac rate generally are unaltered or slightly increased because of increased cardiac output. Increased myocardial contractility may increase myocardial oxygen demand and coronary blood flow.

Mechanism

Synthetic sympathomimeticamine
Overall effect similar to Dopamine with
Selective for Beta1-Adrenergic Receptors,
Increased cardiac contractility and Heart rate
Beta2-Adrenergic Receptors, Mild increase in vasodilation
Does not directly affect renal or splanchnic flow
Relatively mild Alpha1-adrenergic Receptors,effect
Vasoconstriction countered by more potent beta effect
Minimal effects on myocardial oxygen demand
Favorable balance between oxygen supply and demand
Preferred in cardiogenic shock over dopamine
Increased perfusion balances inotropic strain
Benefit lost if not titrated to avoid tachycardia
Does not increase infarct size
Does not elicit arrhythmia

Indications

cardiogenic shock
Often used in combination with Dopamine
• Moderate dosages of each (7.5 ug/kg/min)
• Maintains critical organ perfusion
• Less pulmonary congestion than with Dopamine alone
• Not shown to alter mortality
• May alter secondary organ injury outcomes
Septic Shock
May be useful in enhancing left ventricular function
Epinephrine is preferred agent in Septic Shock
Not usually indicated in non-cardiogenic shock


Adverse Effects
Tachycardia
Arrhythmia
Provokes Myocardial ischemia if tachycardia occurs
Headache
Nausea
Tremor
Hypokalemia

Levosimendan is a calcium sensitiser administered as a single 24 hours continuous intravenous infusion (loading dose: 6-12 µg/kg over 10 minutes followed by a continuous infusion of 0.05-0.1 µg/kg/min). It has several potential advantages, for example it:
Increases the sensitivity of troponin C for Ca2+ and hence the force of contraction
Reduces cardiac filling pressures
Increases the cardiac output without increasing myocardial oxygen requirements (it improves myocardial efficiency)
Causes peripheral and coronary vasodilation with a potential anti-ischaemic effect.

These haemodynamic effects often last longer than the infusion, probably as a consequence of the persistence of an active metabolite. Several studies have evaluated the efficacy of levosimendan in patients with cardiac failure, ischaemic heart disease, or cardiogenic or septic shock.

Preventing oliguria and renal replacement therapy

The most important priority in patients with oliguria is to:
Optimise haemodynamics (renal perfusion pressure and blood flow with fluids and vasoactive drugs)
Correct the underlying cause of shock.


A recent expert opinion document gave the following general recommendations:
Prophylactic volume expansion by isotonic crystalloids using isotonic sodium bicarbonate in patients at risk of contrast nephropathy especially for emergency procedures or theophylline in acute interventions when hydration is not feasible. N-acetylcysteine is not recommended
Peri-procedural continuous veno-venous haemofiltration in an ICU environment to limit contrast nephropathy after coronary interventions in high risk patients with advanced chronic renal insufficiency

Prophylactic use of fenoldopam in cardiovascular surgery patients at risk of acute kidney injury. Avoidance of 10% HES 250/0.5 and higher molecular weight preparations of HES and dextrans in sepsis
The use of low dose dopamine and furosemide is ineffective at preventing kidney injury and the need for renal replacement therapy, and therefore their routine use for this scope should be discouraged.

Glycaemic control

Hyperglycaemia (defined as a blood glucose level >10-11.1 mmol/l) is associated with poor clinical outcomes in critical illness. Tight glycaemic control using intensive insulin therapy (ITT) with continuous intravenous insulin, titrated to maintain glucose <8.3 mmol/l, and ideally between 4.4-6.1 mmol/l, has been associated with a significant reduction in mortality in critically ill surgical patients and in morbidity among all patients in the medical ICU. However, more recent studies in mixed populations of critically ill patients have shown that IIT increases the incidence of severe hypoglycaemia without improving survival. A blood glucose target of ~8 mmol/l seems reasonable in most critically ill patients. This seems to be also true in patients with septic shock receiving corticosteroids.

Specific measures

Septic shock
Updated guidelines on the management of septic shock have recently been published. These guidelines recommend early institution of adjunctive treatment for septic shock, as these strategies result in significant improvement in survival. The strategy includes:
Blood cultures and cultures from other sites of possible infection, prior to antibiotics
Identification and control of a possible source of infection (eg abscess drainage) .

Initial empirical intravenous antibiotic treatment, started within one hour of recognition of sepsis
Steroids (200-300 mg/day of hydrocortisone, for seven days) are to be considered in patients with septic shock on vasoactive drugs
Recombinant activated protein C (rhAPC, Xigris) should be started, in the absence of contraindications, in patients with septic shock with multiple-organ failure.

Patients requiring mechanical ventilation should be managed with “low tidal volume” strategy (6 ml/kg of predicted body weight) in conjunction with an inspiratory plateau pressure of <30 cm H2O. The level of positive end-expiratory pressure is still unclear but it is possible the higher levels are more lung protective than lower levels provided the inspiratory plateau pressure does not exceed 28-30 cm H2O.


Cardiogenic shock
The outcome of patients with acute myocardial infarction complicated by cardiogenic shock depends on prompt coronary revascularisation and managing the low cardiac output state.
Current guidelines recommend:
Early revascularisation with percutaneous coronary intervention or a coronary artery bypass graft (the therapy of choice)
Patients unsuitable for these interventions should receive thrombolysis assisted by vasopressors and an intra-aortic balloon pump,Patients who fail thrombolysis should be considered for rescue angioplasty
Consider bypass grafting when there are associated mechanical complications or in patients with left main or severe three vessel disease.

Early revascularisation, with either PCI or CABG, is the gold standard treatment for patients <75 years old who develop shock within 36 hours of MI and who are suitable for revascularisation that can be performed within 18 hours of shock or in selected patients older than 75 years with good prior functional status.
All patients with cardiogenic shock complicating an AMI should receive aspirin, clopidogrel, heparin, and glycoprotein (GP) IIb/IIIa inhibitors.

Learning bite - anaphylactic shock

For patients with anaphylaxis who are typically hypotensive and short of breath, you should give 0.5 ml intramuscular adrenaline 1:1000.

A low value indicates tissue hypoxia

A low central venous oxygen saturation indicates tissue hypoxia.
Tissue hypoxia may be present in spite of a high central venous oxygen saturation, when oxygen extraction is deficient as a consequence of mitochondrial dysfunction or cellular injury.

There are no data supporting a survival benefit of colloids over crystalloids in the initial management of patients with shock.
A blood transfusion is indicated in people with a haemoglobin level <7.0 g/dl or a haematocrit <30%.
There are no data showing that dopamine improves survival. On the contrary, the SOAP trial showed an increase in risk of death in patients receiving dopamine.
Achieving an ScvO2 >70% has been shown to reduce mortality.


Dobutamine would not be effective as a sole agent in the presence of severe hypotension.
Thrombolysis is ineffective in the presence of hypotension, and giving it before percutaneous coronary intervention has not been shown to be superior to percutaneous coronary intervention alone.
Glyceryl trinitrate would cause further hypotension and is therefore not the vasoactive agent of choice in the presence of severe hypotension.
Early revascularisation with percutaneous coronary intervention or coronary artery bypass grafting is the treatment of choice.

Hypotension is a late sign, and its absence does NOT exclude cardiogenic shock.

Pulmonary congestion, although common, is not universal and therefore its absence does NOT exclude cardiogenic shock.
Patients may have profound diastolic dysfunction and cardiogenic shock in the presence of a normal left ventricular ejection fraction.

Neurogenic

Neurogenic shock is associated with bradycardia and a vasoparalysis with a low central venous pressure.
Septic
Septic shock in the established phase is often characterised by a high cardiac index, high central venous oxygen saturation, and low central venous pressure.
Cardiogenic
Patients usually have hypotension, reduced central venous oxygen saturation, reduced cardiac index, and a raised central venous pressure.

Anaphylactic

Anaphylactic shock is often characterised by a high cardiac index, high central venous oxygen saturation, and low central venous pressure.
Hypovolaemic
Hypovolaemic shock is characterised by a low cardiac index, low central venous oxygen saturation, and low central venous pressure.


A central venous catheter
The oxygen saturation of blood sampled from a central venous catheter is the central venous oxygen saturation.
A peripheral venous line
The oxygen saturation of blood sampled from a peripheral line is generally used to assess global tissue hypoxia.