- Shock occurs when the cardiovascular system is unable to supply adequate amounts of blood and nutrients to the body. This leads to tissue hypoxia
- If shock is not rapidly reversed, organ damage will occur and become irreversible
- The majority of patients with shock require treatment with intravenous fluids
- If initial fluid resuscitation does not work, arrange for invasive haemodynamic monitoring
- When shock is unresponsive to adequate resuscitation with fluids, start inotropic or vasopressor therapy
Shock is not a diagnosis in itself.
It can be defined as acute circulatory failure in which delivery of oxygen to the cells is insufficient to meet the metabolic demands of the tissues.
It results in generalised cellular hypoxia.
If it is not corrected, inadequate tissue perfusion ultimately leads to end organ injury and multiorgan failure.
Shock progresses unless treated.
The aim of resuscitation is to prevent shock worsening and to restore the circulation to a level that meets the oxygen requirements of the body's tissues.
Types of shock
| Table 1: Types of shock | |
| Type of shock | Causes |
| Hypovolaemic: most common | Secondary to fluid loss |
| a. Loss of exogenous fluid |
|
| b. Loss of endogenous fluid through leaks in the microcirculation or into body cavities |
|
| Cardiogenic: caused by impairment of the pump function of the heart |
|
| Distributive: caused by inappropriate vasodilation leading to maldistribution of blood flow |
|
| Obstructive: caused by mechanical impediment to blood flow |
|
Shock with no obvious cause
Occasionally a patient will present with shock with no obvious cause.
Occasionally a patient will present with shock with no obvious cause.
When this occurs, consider:
- Occult haemorrhage, for example:
- Upper gastrointestinal haemorrhage without haematemesis or melaena
- Concealed obstetric or gynaecological loss of blood
- Hidden sepsis, for example:
- Silent intraperitoneal perforation
- Silent cardiovascular events, for example:
- Myocardial infarction in elderly people or patients with diabetes.
CLINICAL FRATURES OF SHOCK
| Table 2: Clinical features of shock | |
| Skin changes* |
|
| Mental changes due to low cerebral perfusion |
|
| Changes in pulse, blood pressure, and urine output ** |
|
| Chemical markers of poor tissue perfusion *** |
|
*In distributive shock, where the
cardiac output is high, the skin is often warm and well perfused,
for example, in septic shock. But in late septic shock, where the
cardiac output is low, the patient is often peripherally cold.
**It is important that you make
every effort to find out a patient's normal blood pressure - in a
hypertensive patient, a normal blood pressure may not adequately
perfuse vital organs such as the kidneys or the brain.
***Poor tissue perfusion of oxygen leads to anaerobic
metabolism which causes lactic acidosis. As a result, shocked
patients may be breathless as a result of respiratory compensation
for the acidosis. |
|
Note:
- Acutely, the body compensates for tissue hypoperfusion by activating the autonomic nervous system. In patients with hypovolaemia, patients can compensate for a reduction of up to 25% of the circulating intravascular volume by increasing endogenous catecholamines. These cause venoconstriction and increase venous return.
- This is we often see tachycardia first before the blood pressure falls in the early stages of patients with shock. Hypotension occurs once the compensatory mechanisms have been overwhelmed or where the autonomic nervous system is unable to respond effectively, for example, patients with autonomic neuropathy or on beta blockers.
Definitions to help understand the causes of shock
Mean arterial pressure is defined as the average pressure throughout the cardiac cycle.
It is equal to diastolic blood pressure + 1/3 (systolic blood pressure - diastolic blood pressure)
Mean arterial pressure = Cardiac output x Systemic vascular resistance + central venous pressure
Since central venous pressure is usually small enough to be neglected in this formula:
Mean arterial pressure ≈ Cardiac output x Systemic vascular resistance
Systemic vascular resistance is the resistance to flow by the peripheral circulation that the heart must overcome to push blood through the circulatory system.
Cardiac output is the volume of blood pumped by the ventricles in a minute. It is normally around 5 litres per minute
Cardiac output = Heart rate x Stroke volume
Stroke volume is the volume of blood ejected in a single ventricular contraction. It is dependent on:
- Preload
- This is equivalent to the ventricular end diastolic volume
- Afterload
- This is the load against which the ventricle has to work
- Myocardial contractility
- This is the amount of mechanical work done by the heart for a given preload and afterload.
Mean arterial pressure ≈ Cardiac output x Systemic vascular resistance
Cardiac output = Heart rate x Stroke volume
From the above definitions and equations, a low blood pressure can occur because of:
- A low cardiac output
- due to a low heart rate or a low stroke volume
- for example, in hypovolaemic shock
- A low systemic vascular resistance
- for example, in distributive shock
Note
- It is important to remember that blood pressure does not reflect cardiac output. A low blood pressure can occur when either the cardiac output or systemic vascular resistance is high. For example, blood pressure can be low:
- With a high cardiac output when systemic vascular resistance is low as in septic shock
- With a high systemic vascular resistance when cardiac output is low as in cardiogenic shock.
INVESTIGATIONS IN SHOCK
Do the following tests:
- Full blood count
- Clotting
- Renal and liver function tests
- Blood cultures
- Troponin level
- Arterial blood gases
- ECG and chest x ray
- Urine, sputum, and blood cultures.
MANAGEMENT OF SHOCK
Do the following:
- Give high flow oxygen via a facemask
- Secure intravenous access
- Arrange for basic monitoring
- non-invasive blood pressure,
- pulse oximetry,
- respiratory rate
- core temperature
- continuous ECG
- Insert a urinary catheter
- Give a fluid challenge.
CLINICAL INDICATIONS FOR A FLUID CHALLENGE
Treat any signs of volume depletion with a fluid challenge.
These signs include:
- Hypotension -
- Mean arterial pressure <65 mm Hg,
- Systolic blood pressure <90 mm Hg
- Oliguria -
- Urine output <0.5 ml per kg per hour
- Tachycardia >100 beats per minute
- Lactic acidosis.
The fluid challenge
Be aware of the difference between an increase in maintenance fluids and a fluid challenge.
An increase in maintenance fluids
This simply increases the rate of administration of continuous fluids. This will not expand the intravascular volume.
A fluid challenge
A fluid challenge describes the initial volume expansion period in which the response of the patient to fluid administration is carefully evaluated.
During this process, give large amounts of fluids over a short period of time under close monitoring to evaluate the patient's response.
When giving a fluid challenge, define:
- The type of fluid to be given
- for example, natural or artificial colloids or crystalloids
- The rate of infusion of fluids
- for example, 500 to 1000 ml over 30 minutes
- The end points
- for example, mean arterial pressure of >65 mm Hg, heart rate of <100 beats per minute
- The safety limits
- for example, development of pulmonary oedema.
1. The type of fluid: Crystalloid or colloid?
Fluids are given into the intravascular fluid compartment. Understanding how long colloids and crystalloids stay in this compartment and how they distribute from the intravascular compartment into the different fluid compartments of the body can help to decide which fluid to give.
The different body compartments
Total body water makes up approximately 50-60% of total body weight.
In a 70 kg man, body water is around 42 litres. Body water is divided into
- Intracellular fluid
- that located inside cells
- two thirds of body water is intracellular fluid.
- Extracellular fluid
- that located outside cells.
- One third is extracellular fluid
- 75% is made up of interstitial fluid
- 25% is made up of plasma/intravascular fluid.
What are crystalloids and how do they distribute within the body fluid compartments?
Crystalloids are water based solutions containing small solutes such as sodium chloride or dextrose.
Examples of crystalloids include:
- 0.9% normal saline - this contains 154 mmol/l of sodium chloride
- 5% dextrose - this contains 50 g/l of dextrose
- Hartmann's solution - this contains 131 mmol/l of sodium; 111 mmol/l of chloride.
Normal saline has a smaller volume of distribution (the volume of body fluid in which the crystalloid/colloid is dissolved) than 5% dextrose. Since normal saline has a sodium concentration similar to that of the extracellular fluid, it only redistributes within the extracellular compartment.
For every 1 litre of normal saline given, about 750 ml redistributes within the extracellular compartment and about 250 ml remains in the intravascular compartment. So, to replace 100 ml of lost fluid, you would need to give 400 ml of normal saline (since 300 ml will redistribute within the extracellular compartment). Excess fluid in the interstitial space leads to oedema.
Five per cent dextrose is rapidly lost from the intravascular compartment. Five per cent dextrose disperses throughout the intra- and extracellular fluid compartments. This is because cells rapidly take up the glucose so the net effect is of giving pure water. Less than 10% stays in the intravascular space so it is of limited use in fluid resuscitation.
For every 1 litre of 5% dextrose given, less than 100 ml remains in the intravascular compartment.
So, to replace 100 ml of lost fluid, you would need to give 1 litre of 5% dextrose (since 900 ml will disperse throughout the intracellular and extracellular compartments.)
The main disadvantage of crystalloids is that when used to replace massive loss of fluid, they cause peripheral oedema and occasionally pulmonary oedema.
What are colloids and how do they distribute within the body fluid compartments?
Colloids are water based solutions containing large solute molecules such as albumin or starches that cannot easily diffuse out of blood vessels, provided capillary integrity is intact. They exert an oncotic pressure, which pulls water into the intravascular compartment.
They remain in the intravascular compartment for much longer than crystalloids and therefore expand the intravascular volume more quickly than crystalloids. So the volume infused initially stays almost entirely within the intravascular compartment.
Colloids can be natural or synthetic and include:
- Natural: blood, albumin
- Synthetic: for example, gelatins, such as gelofusine or haemacel, starches such as hetastarch.
- Risk of pulmonary oedema and respiratory failure, particularly when capillary permeability is increased, for example, septic patients with leaky capillaries
- Interference with coagulation
- Risk of anaphylactic or transfusion reactions.
Which is better for resuscitation?
Meta-analyses of clinical studies comparing crystalloid and colloid resuscitation in general and surgical patients indicate no difference in clinical outcome between colloids and crystalloids.
As the volume of distribution is much larger for crystalloids than for colloids, resuscitation with crystalloids requires more fluid to achieve the same goals and results in more oedema.
The replacement fluid that is chosen depends in part on the type of fluid that has been lost. Crystalloids are effective at replacing depleted extracellular fluid. For example, in severe vomiting or diarrhoea, diabetic ketoacidosis, or bowel obstruction, assume that depletion of salt and water have caused the hypovolaemic shock. Normal saline is the most commonly used crystalloid but Hartmann's solution has been shown to be less likely than normal saline to cause a hyperchloraemic acidosis.
Colloids are effective at restoring circulating blood volume in severe acute volume depletion, for example, in patients with haemorrhage, burns, or severe sepsis. Although there is no evidence to support 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.
2. The rate of infusion
Give a fluid challenge of 500 to 1000 ml of crystalloid solution or 300 to 500 ml of colloid via a wide bore cannula over 15 to 30 minutes.
3. The end points
Reassess the patient after each fluid challenge. Look for an improvement in:
- Peripheral perfusion
- Mental status
- Heart rate
- aim for heart rate <100 beats per minute
- Blood pressure
- aim for systolic blood pressure >90 mm Hg or mean arterial blood pressure >65 mm Hg.
- Remember, if the patient has hypertension, aim for their normal blood pressure
- Urine output
- aim for >0.5 ml per kg per hour.
4. The safety limits
Although there is no restriction on the amount of fluid that is used, when giving or repeating a fluid challenge, as well as watching the response, watch how the patient tolerates the challenge - look for evidence of intravascular volume overload such as pulmonary oedema.
Note:
- Patients with underlying cardiac disease are more likely to develop pulmonary or peripheral oedema. Give the lower volume of fluid recommended for a fluid challenge in these patients and watch the response carefully.
SHOULD YOU ALWAYS GIVE A FLUID CHALLENGE?
Hypovolaemia is present in most patients with any type of shock. The goal of early resuscitation is to restore the intravascular volume to increase cardiac output and oxygen delivery to the tissues. A fluid challenge will lead to an improvement in most conditions, including myocardial infarction without left ventricular failure.
A fluid challenge may be harmful in cardiogenic shock. If cardiogenic shock is diagnosed, call for senior help. Acute myocardial infarction is the most common cause of cardiogenic shock. The treatment of choice of cardogenic shock complicated by myocardial infarction is early revascularisation with percutaneous coronary intervention or a coronary artery bypass graft.
Evaluating the response to treatment and calling for help
After the initial fluid challenge, if the vital signs:
- Return to normal
- continue monitoring the patient to ensure stability
- Transiently improve
- repeat the fluid challenge, provided there are no signs of pulmonary oedema.
- If there are signs of pulmonary oedema, call for help.
- Do not improve after repeated boluses up to an initial resuscitation volume of 20 to 40 ml/kg of crystalloids (about 1400 to 2800 ml in a 70 kg man) and approximately 5 ml/kg (about 350 ml in a 70 kg man) of colloids
- call for help.
- If there is no improvement in blood pressure despite adequate fluid resuscitation, inotropic support may be required.
- Haemodynamic parameters, that is, blood pressure decreasing, heart rate increasing
- The patient's conscious level
- The chemical markers of poor tissue perfusion, that is, an increasing metabolic acidosis and lactate level.
What happen next?
- An arterial line should be inserted for invasive arterial blood pressure monitoring. Non-invasive monitoring is inaccurate at low pressures and is not sufficiently responsive to guide the minute by minute changes in the management of shock
- A central venous line should be inserted to assess the degree of filling of the venous circulation by using a fluid challenge monitored by central venous pressure
- Before insertion of a central line, a minimum fluid challenge of 20 ml per kg of crystalloid or approximately 5 ml per kg of colloid have been given
- The patient should be transferred to a high dependency unit or intensive care unit
WHAT DOES THE CENTRAL VENOUS PRESSURE MEASURE?
The central venous pressure is usually measured in the superior vena cava via a cannula inserted into the internal jugular or subclavian veins. It reflects the mean right atrial pressure and is frequently used as an estimate of right ventricular preload and to estimate the intravascular volume.
Limitations of measurement of central venous pressure
Normal central venous pressure is variable and depends on:
- Intravascular volume
- Venous tone
- Ventricular compliance
- Intrathoracic pressure
- Position of the patient
- An intact tricuspid valve.
Right sided heart pressures do not always equate with left sided pressures, especially in ill patients. Therefore, the central venous pressure may not provide a reliable index of left ventricular preload, which is the main determinant of cardiac output. The central venous pressure can:
- Overestimate the left ventricular pressure
- for example, in a patient with right heart failure secondary to chronic obstructive pulmonary disease, the central venous pressure will be high and not reflect the left ventricular pressure which may be normal
- Underestimate the left ventricular pressure
- for example, in a patient with an impaired left ventricle secondary to a myocardial infarction, the central venous pressure may be within the normal range (8-12 cm) reflecting comparatively normal right ventricular function and not reflecting the left ventricular filling pressure, which may be high.
WORKED EXAMPLE
A 56 year old man has had a large anterior myocardial infarction. His blood pressure is 95/55 mm Hg. His initial central venous pressure was 6 cm. A fluid challenge led to a transient rise in the central venous pressure to 8 cm. The medical registrar thought that he was under filled and gave another fluid challenge. The patient became breathless. Clinical and chest x ray examination confirmed pulmonary oedema. What has happened?
It is likely that this patient has an impaired left ventricle secondary to his myocardial infarction. Therefore the central venous pressure reading reflected a comparatively normal right ventricular function and did not reflect the left ventricular filling pressure, which was probably high. Therefore the repeat fluid bolus led to pulmonary oedema.
Response of central venous pressure to a fluid challenge
 |
| Figure 2: Response of central venous pressure to a fluid challenge (From Acute care: Volume resuscitation. StudentBMJ 2004) |
The table below explains how to interpret the response of central venous pressure to a fluid challenge shown in Figure 2
| Change in central venous pressure | Clinical interpretation | Action |
| Transiently rises then returns to pre challenge pressure | Implies that the patient remains underfilled despite the fluid challenge | Give another fluid challenge |
| Rises and the rise is sustained above the pre challenge pressure | Implies that the patient is adequately filled | Monitor patient closely |
| Rises and remains high following the challenge | Implies that the patient is overfilled | Monitor patient closely. Diuretics may be necessary |
Response of the central venous pressure to successive fluid challenges
When successive fluid challenges are given, watch the trend in the central venous pressure and monitor the patient closely for pulmonary oedema.
When the patient is adequately filled, a sustained rise in central venous pressure of more than 3 cm occurs. At this point, stop the fluid challenges and reassess the patient.
Adequate fluid replacement should produce a sustained rise in central venous pressure together with an improvement in heart rate, blood pressure, and urine output. If there is no improvement in blood pressure or urine output despite adequate fluid resuscitation leading to a sustained rise in central venous pressure, inotropic support may be required.
WORKED EXAMPLES
1. A 75 year old woman was admitted to the medical admissions unit with a urinary tract infection. She was kept in because she had been vomiting and was not able to tolerate oral antibiotics.
Overnight, her condition deteriorated. She became warm and peripherally vasodilated. Her pulse increased from 90 to 120 beats per minute, her blood pressure dropped from 110/65 mm Hg to 85/50 mm Hg, and her temperature increased from 37.8º to 39ºC.
The medical admissions unit doctor thinks she has hypovolaemic shock secondary to her reduced oral intake and vomiting. Your registrar thinks she has now gone into septic shock secondary to her urinary infection.
Who do you think is closer to the truth?
Your registrar. Although her oral intake is poor and she has vomited, she is warm, dilated, and pyrexial. The shock is much more likely to be caused by sepsis rather than hypovolaemia. But remember, in late septic shock, or in patients with vascular disease, a patient can be peripherally cold and shut down.
You give high flow oxygen via a facemask, arrange for basic monitoring, insert a urinary catheter, and repeat cultures. After she fails to respond to two fluid challenges of 500 ml of gelofusine, the registrar inserts a central line.
Was he right to insert a central line?
Yes. She did not respond to 1000 ml of gelofusine. You should give a minimum fluid challenge of 20 ml per kg of crystalloid or approximately 5 ml per kg of colloid before you insert a central line.
After the central line was inserted, the patient suddenly became acutely breathless. The central venous pressure rose to 18 cm. The blood pressure remained at 85/50 mm Hg.
What do you think has happened?
The central line may have caused a tension pneumothorax. Obstructive shock in addition to septic shock has probably developed. This accounts for the rise in the central venous pressure. The tension pneumothorax has caused the mediastinum to shift, impeding venous return and cardiac output.
2. A 58 year old man with Crohn's disease has been admitted following three days of severe diarrhoea. He feels cool. His pulse is 130 beats per minute and his blood pressure is 80/50 mm Hg. What sort of shock is he in?
Hypovolaemic shock. The history of loss of exogenous fluid, his cool extremities, and haemodynamic parameters point to hypovolaemic shock.
What would you do next?
Give him a fluid challenge of either 500 to 1000 ml of crystalloid or 300 to 500 ml of colloid over 15 to 30 minutes. Since crystalloids are more effective at replacing depleted extracellular fluid and Hartmann's solution has been shown to be less likely than normal saline to cause a hyperchloraemic acidosis, Hartmann's solution would be a good choice here.
Following the challenge, reassess him against specific endpoints, for example, systolic blood pressure >90 mm Hg, pulse <100 beats per minute.
After the challenge, his blood pressure and pulse remain unchanged. He has become confused and a blood gas shows that he now has a metabolic acidosis.
What would you do next?
Call for senior help
His deterioration following treatment indicates the need for invasive haemodynamic monitoring and repeated intravenous fluid challenges with guidance by central venous pressure measurements. Transfer to a critical care area is also important.
He is transferred to the high dependency unit, where the doctors insert a central line. The initial measurement is 2 cm. He is given a further intravenous fluid challenge. The central venous pressure initially increases to 4 cm and then drops back to 2 cm after 10 minutes.
What would you do next?
The central venous pressure response to the fluid challenge implies that he is under filled. You should repeat the fluid challenges until a sustained rise in central venous pressure occurs, provided pulmonary oedema does not develop.
FURTHER READINGS:
- Practice parameters for haemodynamic support of sepsis in adult patients in sepsis. Task Force of the American College of Critical Care Medicine, Society of Critical Care Medicine. Crit Care Med 1999;27:639-60.
- Levy MM, Fink MP, Marshall JC, et al. 2001 SC CM/ESI CM/ACCP/ATS/SIS international sepsis definitions conference. Intensive Care Med 2003;29:530-8
- Graham CA, Parke TRJ. Critical care in the emergency department: shock and circulatory support. Emerg Med J 2005;22:17-21
- Dellinger RP, Carlet JM, Masur H, Gerlach H, Calandra T, Cohen J, et al. Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Intensive Care Med 2004;30(4):536-55. http://www.survivingsepsis.com.
- Choi PTL, Yip G, Quinonez LG, et al. Crystalloids vs. colloids in fluid resuscitation: A systematic review. Critical Care Med 1999;27:200-10.
- Schierhout G, Roberts I. Fluid resuscitation with colloid or crystalloid solutions in critically ill patients: A systematic review of randomised trials. BMJ 1998;316:961-964.
- Kellum JA. Saline-induced hyperchloremic metabolic acidosis. Crit Care Med 2002;30(1):259-61
- Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction--executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2004;44(3):671-719.
- American Thoracic Society. Evidence-based colloid use in the critically ill: American Thoracic Society Consensus Statement. Am J Respir Crit Care Med 2004;170(11):1247-59.
- Cooper N. Response of central venous pressure to a fluid challenge picture (4) Acute care: Volume resuscitation. studentBMJ 2004;12:133-76.
- Endocrine system. The British National Formulary March 2007.
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