Shock

• Diagnosis of shock is based on the clinical appreciation of presence of inadequate organ perfusion and tissue oxygenation.  This is the 1st step in managing shock.
• Definition of shock is an abnormality of the circulatory system that results in inadequate organ perfusion and tissue oxygenation.
• The second step in managing shock is to identify cause.  Most is hypovolaemic (haemorrhage is commonest cause of shock in injured patient), but may be due cardiogenic, neurogenic, septic (especially if arrival delayed) causes.  In addition tension pneumothorax can reduce venous return and produce shock (should be considered in patient with injuries above the diaphragm).
• Neurogenic shock results from extensive injury to the CNS or spinal cord, NOT FROM ISOLATED BRAIN INJURIES.

Basic cardiac physiology

Cardiac Output (CO) is defined as volume of blood pumped by heart per minute and is determined by product of heart rate and stroke volume:

CO = HR * SV

• Stroke volume is determined by preload, myocardial contractility and afterload.
• Preload denotes volume of venous return to the heart and is determined by venous capacitance, volume status and difference between mean venous systemic pressure and right atrial pressure (which determines venous flow).
• The venous system can be considered a reservoir or capacitance system in which the volume of blood can be divided into 2 components:
• Component that doesn’t contribute to mean systemic venous pressure and represents the volume of blood that would remain in this capacitance circuit if the pressure were 0.
• The 2nd more important component represents the venous volume that contributes to the mean systemic venous pressure.

• Nearly 70% of the total blood volume is estimated to be located in the venous circuit.
• The relationship between the venous volume and venous pressure describes the compliance of the system.  It is this pressure gradient that drives venous flow and therefore the volume of venous return to the heart.
• BLOOD LOSS REDUCES THE 2ND COMPONENT OF VENOUS VOLUME, REDUCES THE PRESSURE GRADIENT AND REDUCES VENOUS RETURN.
• The volume of venous blood returned to the heart determines myocardial muscle fibre length after ventricular filling at end-diastole.
• Muscle fibre length is related to the contractile properties of myocardial muscle according to Starling’s law.
• Myocardial contractility is the pump that drives the system.
• Afterload is systemic (peripheral) vascular resistance

Blood loss pathophysiology

Early circulatory responses to blood loss are compensatory:

• Progressive vasoconstriction of cutaneous muscle, visceral circulation to preserve blood flow to the kidneys, heart and brain.
• Increased heart rate to preserve CO, and is often the earliest measurable sign.
• Release of endogenous catecholamines increases diastolic blood pressure and reduces pulse pressure, BUT DOES LITTLE TO IMPROVE ORGAN PERFUSION.
• Other vasoactive hormones (histamine, bradykinin, beta-endorphins and a cascade of prostanoids and other cytokines) are released and have a profound effect on microcirculation and vascular permeability.
• These compensatory mechanisms preserve venous return initially by contraction of the volume of blood in the venous system (not contribute to mean venous systemic pressure).  This is limited, the most effective method to restore adequate cardiac output and end organ perfusion is to restore venous return by volume repletion.
• At cellular level cells are deprived of essential substrates for normal aerobic metabolism and energy production.  Initial compensation is by anaerobic metabolism forming lactic acid and development of metabolic acidosis.
• If shock is prolonged substrate delivery for the generation of adenosine triphosphate (ATP) is inadequate, the cellular membrane loses the ability to maintain its integrity and normal electrical gradient is lost (Na-K pump doesn’t work).
• Swelling of the endoplasmic reticulum is first evidence of cellular hypoxia, mitochondrial damage soon follows.  Lysosomes rupture releasing digestive enzyme.  Sodium and water enter cell and it swells.  Intracellular calcium deposition occurs.
• If the process isn’t reversed progressive damage occurs, additional tissue swelling and then cellular death.  THIS COMPOUNDS IMPACT OF BLOOD LOSS AND HYPOPERFUSION.
• Administration of isotonic electrolyte solutions helps combat this process.
• Management is to reverse this phenomenon by providing adequate oxygenation, ventilation and appropriate fluid resuscitation.
• Resuscitation may be accompanied by marked increase in interstitial oedema, which is caused by “reperfusion injury” to capillary interstitial membrane.  Resulting in more fluid than thought being required.
• In haemorrhagic shock treatment is to increase preload, VASOPRESSORS ARE CONTRAINDICATED.
• PRESENCE OF SHOCK IN AN INJURED PATIENT DEMANDS INVOLVEMENT OF SURGEON AS REQUIRE EARLY SURGICAL INTERVENTION TO REVERSE SHOCK STATE.

Initial patient assessment

A) Recognition of shock

• After airway is assured it is important to identify manifestations of shock that include tachycardia and cutaneous vasoconstriction.  ACCORDINGLY ANY PATIENT WHO IS COOL AND TACHYCARDIC IS IN SHOCK UNTIL PROVE OTHERWISE.
• Sole reliance on blood pressure results in delayed recognition of the shock state.  There is no measurable fall in blood pressure till 30% of blood volume is lost due compensatory mechanisms.
• Check pulse rate, respiratory rate, skin circulation and pulse pressure.
• Heart rate varies with age.  Tachycardia if > 160 in an infant, > 140 in pre-school, >120 to puberty and >100 in adult.  Elderly patient may not demonstrate tachycardia due limited reserve, or slowing drugs, or pacemaker.
• A narrowed pulse pressure suggests significant blood loss and involvement of compensatory mechanisms.
• Use of haematocrit or Hb concentration is unreliable and inappropriate for diagnosing shock.  Thus a very low haematocrit obtained shortly after injury suggests massive blood loss or a pre-existing anaemia, while normal haematocrit doesn’t exclude significant blood loss.

B) Clinical differentiation of aetiology of shock

• May be classified as haemorrhagic or non-haemorrhagic.
• Be aware of tension pneumothorax in patient with injuries above diaphragm.
• Needs appropriate history and careful examination.
• Additional tests may confirm suspicions but shouldn’t delay aggressive volume restoration.

a. Haemorrhagic shock:

• This is the commonest cause of shock after injury.
• Most non haemorrhagic shock states respond initially or partially to volume resuscitation.
• IF SIGNS OF SHOCK ARE PRESENT TREATMENT AS HYPOVOLAEMIC.

b. Non-haemorrhagic shock:

1. cardiogenic shock:
   • From blunt injury, cardiac tamponade, air embolus or MI.
   • Blunt injury should be suspected when mechanism of injury is rapid deceleration.  All blunt injuries require ECG monitoring.  Blood CPK isoenzymes rarely have any value.  Blunt injury may be indication for early CVP monitoring.
   • Cardiac tamponade is most common in penetrating thoracic trauma, but may be due blunt injury.  Tachycardia, muffled heart sounds and dilated engorged neck veins with hypotension resistant to fluid treatment suggest cardiac tamponade.  ABSENCE OF THESE DOESN’T EXCLUDE THIS CONDITION.
   • Tension pneumothorax may mimic the above but is differentiated by ABSENT BREATH SOUNDS AND HYPERRESONANCE.
2. Tension pneumothorax:
   • Surgical emergency.
   • Develops when air enters the pleural space but a flap-valve mechanism prevents its escape.  Intrapleural pressure rises causing total lung collapse and a shift of mediastinum to opposite side with subsequent impairment of venous return and fall in CO.
   • Presence of acute respiratory distress, subcutaneous emphysema, absent breath sounds, hyperresonance to percussion and tracheal shift supports diagnosis.
3. Neurogenic shock:
   • Isolated intracranial injuries don’t cause shock, if head injury search for another cause.
   • Spinal cord injury may cause shock due loss of sympathetic tone.
   • Classical picture is hypotension without tachycardia or cutaneous vasoconstriction.
   • A narrowed pulse pressure is not seen in neurogenic shock.
   • Treatment is initially for hypovolaemia as usually is concurrent torso trauma.  Failure to restore organ perfusion with fluid replacement suggests either continuing haemorrhage or neurogenic shock.
   • CVP monitoring can be helpful.
4. septic shock:
   • Shock due infection immediately after injury is uncommon, but may occur if delay in reaching hospital of several hours.
   • In patient with penetrating abdominal injuries and contamination of the peritoneal cavity.
   • Septic patient who are hypotensive and afebrile are clinically difficult to distinguish from those in hypovolaemic shock.
   • Patient in early septic shock may have normal circulating volume, modest tachycardia, warm pink skin, near normal systolic pressure and a wide pulse pressure.

Haemorrhagic shock in the injured patient

MOST COMMON CAUSE OF SHOCK IN THE TRAUMA PATIENT.

A. Definition of haemorrhage

• Acute loss of circulating blood volume.
• Normal is about 7% of body weight.  The blood volume of obese patient is estimated on their ideal body weight.
• In child this is 8-9% of body weight.

B. Direct effects of haemorrhage

• 4 classes of haemorrhagic shock, but volume replacement should be directed by response to initial therapy rather than by relying on the initial classification.
• It is dangerous to wait till the trauma patient fits a precise physiologic classification of shock before initiating aggressive volume restoration.  Fluid resuscitation must be initiated when early signs and symptoms of blood loss are apparent or suspected, not when the blood pressure is falling or absent.
• Several confounding factors alter the classic haemodynamic response to an acute loss of blood.  These are:
• Patient age.
• Severity of injury, with special attention to type and anatomical location of injury.
• Time lapse before treatment.
• Prehospital fluid treatment and application of pneumatic antishock garment.
• Medications used for chronic conditions.

1. Class I – blood loss up to 15%:
   • Example: donation of 1 unit blood.
   • Minimal tachycardia.
   • No changes in blood pressure, RR or pulse pressure.
   • Normally not require fluid replacement as will be restored in 24 hours, but in trauma correct.
2. Class II – 15-30% blood volume loss:
   • Uncomplicated haemorrhage requiring crystalloid resuscitation.
   • Represents about 750 – 1500 ml of loss.
   • Tachycardia, tachypnoea and a decrease in pulse pressure (due rise in diastolic component due action of catecholamines).
   • Minimal systolic pressure changes.
   • Anxiety, fright or hostility.
   • UO is only mildly affected.
   • Can usually be stabilised by crystalloid, but may later require blood transfusion.
3. Class III – 30-40% blood volume loss:
   • Complicated haemorrhagic state in which at least crystalloid and probably blood replacement are required.
   • Classical signs of inadequate perfusion, marked tachycardia, tachypnoea, significant changes in mental state and measurable fall I systolic pressure.
   • Almost always require blood transfusion, but decision based on patient initial response to fluid resuscitation.
4. Class IV - > 40%:
   • Preterminal event patient will die in minutes.
   • Marked tachycardia, significant depression in systolic pressure and very narrow pulse pressure (or unobtainable diastolic pressure).
   • UO is negligible.
   • Mental state is markedly depressed.
   • Skin cold and pale.
   • Need rapid transfusion and immediate surgical intervention.
   • Loss of >50% results in loss of consciousness, pulse and blood pressure.

Example of use:
70kg man presents with hypotension. Must be class III at least. Blood requirement is 70 * 7% * 30% = 1470 ml of blood loss.  Using 3 for 1 rule he needs 4.4 litres of crystalloid for resuscitation.  IF PATIENT DOESN’T DEMONSTRATE NORMALISATION OF VITAL SIGNS IN RESPONSE TO THE ADMINISTRATION OF THIS VOLUME, CONSIDER POTENTIAL FOR ONGOING BLOOD LOSS, SHOCK STATE NOT BEING DUE HYPOVOLAEMIA OR ADDITIONAL LOSSES HAVE COMPLICATED PICTURE.

C. Fluid changes secondary to soft-tissue injury

• Major soft tissue injuries and # compromise the haemodynamic status in 2 ways:
• Blood lost into site of injury.  ESPECIALLY PELVIC # LOSS OF BLOOD IN RETROPERITONEAL HAEMATOMA.
• Obligatory oedema occurring in injured tissues.  Tissue injury results in the activation of systemic inflammatory response and production of multiple cytokines, many of which have profound effects of increasing vascular permeability.

Initial management of haemorrhagic shock

The basic management principle is to stop the bleeding and replace the volume loss.

A. Physical examination.

• Includes assessment of the ABCDE’s.
• Baseline recordings are important to monitor the patient’s response to therapy.  Vital signs, UO and level of consciousness are essential.

a. Airway and breathing:

• Establishing airway and adequate ventilation is usual priority.  Aim is to maintain oxygen saturation greater than 95%.

b. Circulation – haemorrhage control:

• Control obvious haemorrhage by direct pressure to bleeding site.
• Obtain adequate iv access and assess tissue perfusion.
• The adequacy of tissue perfusion dictates the amount of fluid resuscitation required.
• Operative control of bleeding may be required.
• PSAG may be used to control bleeding in pelvic or lower extremity injuries, but use shouldn’t interfere with adequate fluid resuscitation.

c. Disability – neurologic examination:

• Brief neurologic examination to determine level of consciousness, eye movements and pupillary response, best motor response and degree of sensation.
• The above is useful in assessing cerebral perfusion.
• Alterations in CNS function in hypotensive patient may reflect inadequate cerebral perfusion and this must be restored before ascribing to intracranial injury.

d. Exposure – complete examination:

• Examine head to toe.
• Prevention of hypothermia is essential.

e. Gastric dilatation – decompression:

• Occurs often, ESPECIALLY IN CHILD, and may cause unexplained hypotension or cardiac dysrhythmia (usually bradycardia) from EXCESSIVE VAGAL STIMULATION.
• Gastric distension makes shock difficult to treat.  In the unconscious patient, gastric dilatation increases the risk of aspiration.
• Decompression is accomplished by intubating the stomach with a tube passed nasally or orally and attaching it to suction to evacuate gastric contents, BUT DOESN’T REMOVE RISK OF ASPIRATION TOTALLY.

f. Urinary catheter insertion:

• Allows assessment of urine for haematuria and monitoring of UO.
• Blood at urethral meatus, a high-riding prostate/non-palpable prostate in male is absolute contraindication to the insertion of a transurethral catheter prior to radiographic confirmation of an intact urethra.  (See abdominal trauma chapter).

B.Vascular access lines.

• Should be done promptly with minimum of 16 gauge peripheral iv catheters before any consideration is given to a CV line.
• Rate of flow is proportional to the fourth power of the radius of the cannula and inversely proportional to its length (Poiseuille’s law).  Hence short large diameter cannulae are preferred.
• Most desirable sites are forearm or antecubital veins.  If conditions prevent use here, large calibre, central venous (femoral, jugular or subclavian) access using Seldinger technique or saphenous vein cutdown is indicated.  These lines should be changed to more appropriate lines as soon as the situation warrants.  Consideration should be given to the potential for serious complications related to attempted CVP placement.
• In child <6 an intraosseous needle should be attempted before CVP.
• As iv lines are started blood samples are drawn for type and crossmatch, appropriate laboratory tests, toxicology studies and testing of all females of childbearing age for pregnancy.  ABG should be obtained now.
• CXR should be obtained post insertion of subclavian/CVP to check position and for pneumo or haemothorax.

C.Initial fluid therapy.

• Isotonic electrolyte solutions for initial resuscitation, this provides transient intravascular expansion and further stabilises the vascular volume by replacing fluid losses into the interstitial and intracellular spaces.
• Ringer’s lactate is treatment of choice initially, normal saline is second choice (but has potential to cause hyperchloraemic acidosis, especially if renal function is impaired).
• Initial fluid bolus is given as rapidly as possible.  The usual dose is 1-2 litres for adult and 20ml/kg in paediatric patient.
• A rough guideline for total amount of crystalloid acutely required is 3 to 1, but it is more important to assess the patient’s response to fluid resuscitation (UO, peripheral perfusion and level of consciousness).
• If amount of fluid required is much above this then re-evaluate for other causes of shock or unrecognised injuries.

Estimated fluid and blood losses based on initial presentation.

Evaluation of fluid resuscitation and organ perfusion

A.General.

• The return of normal blood pressure, pulse pressure and pulse rate are positive signs that suggest perfusion is returning to normal, BUT GIVE NO INFORMATION OF ORGAN PERFUSION.
• Improvements in CNS status and skin circulation are important evidence of enhanced perfusion but are difficult to quantitate.  Normal UO generally imply adequate renal blood flow IF NO DIURETICS and as such is prime monitor of resuscitation.
• CVP changes can help too, and in difficult cases risks of placement are justified.

B. UO

• May be used as monitor of renal blood flow.
• 0.5ml/kg/hr in adults, 1ml/kg/hr in child, 2ml/kg/hr in those <1yr.
• Decreasing UO with increasing specific gravity suggests inadequate resuscitation.

C.Acid base balance.

• Patient in early hypovolaemic shock have respiratory acidosis due tachypnoea.  This is frequently followed by mild metabolic acidosis that doesn’t require treatment.
• Severe metabolic acidosis may follow due inadequate tissue perfusion and production of lactic acid.
• Persistent metabolic acidosis is usually due inadequate resuscitation or ongoing blood loss.  In normothermic patient should be treatment with fluids, blood and consideration of operative intervention for control of haemorrhage.
• Sodium bicarbonate should not be used routinely for treatment of acidosis secondary to hypovolaemic shock.

Therapeutic decisions based on response to initial fluid resuscitation

• Patient response to initial fluid resuscitation is key to determining subsequent therapy AFTER ABCDE’s AND RESUSCITATION.
• May identify those whose blood loss was greater than estimated or those with ongoing fluid loss.
• Haemodynamically stable patient is one who is under resuscitated and still in shock.
• Haemodynamically normal patient has no signs of inadequate tissue perfusion.
• 3 potential response patterns to resuscitation:

A.rapid response:

• Respond rapidly and remain haemodynamically normal once fluid bolus given.
• Lost less than 20% and no further fluid bolus or immediate blood administration is indicated.
• Surgical consultation and evaluation are necessary during initial assessment and treatment, as operative intervention may still be necessary.

B.Transient response:

• Responds to initial fluid bolus but begin slow deterioration as initial fluids are slowed to maintenance levels.
• This is ongoing blood loss or inadequate resuscitation.
• Lost 20-40% initially.
• Continued fluid administration and initiation of blood transfusion are indicated.

C.Minimal or no response:

• Dictates need for immediate surgical intervention to control haemorrhage.
• On rare occasions failure to respond may be due to pump failure as a result of blunt cardiac injury or cardiac tamponade.  THESE DIAGNOSES SHOULD ALWAYS BE CONSIDERED IN THESE PATIENTS.
• CVP or echocardiography helps in diagnosis.

Blood replacement

A.packed red blood cells versus whole blood treatment:

• Either whole blood or packed red blood cells may be used to resuscitate the trauma patient.
• Main purpose of blood is to restore oxygen carrying capacity of the intravascular volume.
• Volume resuscitation itself can be accomplished with crystalloids, with the added advantage of contributing interstitial and intracellular volume restitution.

B.Crossmatched, type-specific and type O blood:

• Fully crossmatched blood is preferable, but takes 1 hour.
• Type specific blood can be provided within 10 minutes.  Such blood is compatible with ABO and Rh blood types but other Ab incompatibilities may exist.
• Type specific blood is preferred for transient responders.
• If type-specific is required crossmatching should be completed by blood bank.
• Type O packed cells can be used if above not available.  To avoid sensitisation and future complications Rh-negative cells are preferred for females of childbearing age.
• FOR LIFE THREATENING BLOOD LOSS UNMATCHED, TYPE SPECIFIC BLOOD IS PREFERRED OVER TYPE O BLOOD UNLESS MULTIPLE UNIDENTIFIED CASUALTIES ARE BEING TREATED SIMULTANEOUSLY AND THE RISK OF INADVERTENTLY ADMINISTERING THE WRONG UNIT OF BLOOD TO PATIENT IS GREAT.

C.Warming fluids – plasma and colloid:

• Hypothermia must be prevented and reversed if patient is hypothermic upon arrival at hospital.
• Use of blood warmers is cumbersome yet desirable.
• Heat to 39°C before using it is alternative by storing in warmer or use of microwave.
• Remember blood products cannot be heated in microwave but need a warmer.

D.Autotransfusion:

• Collection of shed blood for autotransfusion should be considered in any patient with a major haemothorax.

E.Coagulopathy:

• Rare in 1st hour of treatment.
• Massive transfusions with resultant dilution of platelets and clotting factors along with the adverse effect of hypothermia on platelet aggregation and clotting cascade are usual causes of coagulopathies in the injured patient.
• INR, APPT and platelet count are valuable markers to obtain in 1st hour, especially if there is a history of coagulopathy, or anticoagulants.
• Transfusion of platelets, cryoprecipitate and ffp should be guided by these coagulation parameters, including fibrinogen.
• Patient with major closed head injury (diffuse axonal injury) are particularly prone to the development of coagulation abnormalities as a result of substances, especially tissue thromboplastin, released by damaged neural tissue.  Should have their coagulation parameters closely monitored.

F.Calcium administration:

• Most don’t need excessive calcium supplements if receiving blood transfusions.

Special considerations in the diagnosis and treatment of shock

A.Equating blood pressure with CO.

• Blood pressure = CO * SVR (bastardisation of Ohm’s law).
• Remember CO not mean tissue perfusion or oxygenation.

B.Age.

• Ageing process produces a relative decrease in sympathetic activity with respect to the cardiovascular system, thought due deficit in receptor response to catecholamines.
• Cardiac compliance decreases with age.  Older patients are unable to increase HR or the efficiency of myocardial contraction when stressed by hypovolaemia.
• Atherosclerotic vascular occlusive disease makes many vital organs extremely sensitive to slightest reduction in blood flow.
• Many patient have pre-existing volume depletion 2 to chronic diuretic use or subtle malnutrition.
• Beta-adrenergic blockade may mask tachycardia as early indicator of shock.
• THUS PRUDENT TO CONSIDER EARLY INVASIVE MONITORING IN THESE PATIENTS.
• Reduction in pulmonary compliance, decrease in diffusion capacity and general weakness of muscle of respiration limit ability of elderly to meet increased demands for gas exchange.  This compound cellular hypoxia already produced by reduction in local oxygen delivery.
• Glomerular and tubular senescence in kidney reduces ability of elderly to preserve volume in response to release of stress hormones.  It is also more susceptible to effects of reduced blood flow and nephrotoxic agents.
• Mortality and morbidity rates increase directly with age, but majority will return to their preinjury status with prompt, aggressive resuscitation and careful monitoring.

C.Athletes

• Blood volume can increase 15-20%.
• CO can increase 6 fold.
• Stroke volume can increase by 50%.
• Resting pulse is generally 50.
• Remarkable ability to compensate for blood loss and may mask usual responses to blood loss.

D.Pregnancy

• Physiological maternal hypervolaemia requires a greater blood loss to manifest hypovolaemia in mother.
• This may be reflected by decreased foetal perfusion.

E.Medications

• Beta-adrenergic blockers and calcium channel blockers can alter the response to haemorrhage.
• Insulin overdosing may be responsible for hypoglycaemia.
• Chronic diuretic therapy may explain unexpected hypokalaemia.
• NSAIDs may adversely affect platelet function.

F.Hypothermia.

• Patient with hypothermia and hypovolaemia don’t respond normally to administration of blood and fluid resuscitation and often develop COAGULOPATHY.
• As such body temperature monitoring is important.  Bladder or oesophageal temperature is an accurate clinical measure of core temperature.
• Hypothermia is best treated by prevention.
• See injuries due to burns or cold chapter.

G.Pacemaker

• Patients are unable to respond to blood loss in expected fashion and CVP monitoring is invaluable in these patients to guide fluid therapy.

Reassessing patient response and avoiding complications

Inadequate volume replacement is most common complication of haemorrhage shock.

A.Continued haemorrhage.

• Obscure haemorrhage is most common cause of poor patient response to fluid.

B.Fluid overload and CVP monitoring.

• Risk of fluid overload is minimised by monitoring the patient carefully.
• Remember the goal is restoration of organ perfusion and adequate tissue oxygenation, which is confirmed by appropriate UO, CNS function, skin colour and return of pulse and blood pressure toward normal.
• Early transfer to ITU in patients with non haemorrhagic causes of shock and elderly patients.
• CVP monitoring is relatively simple procedure and is used as a standard guide for assessing ability of right side heart to accept a fluid load.  Points to remember are:

1. The precise measure of cardiac function is the relationship between ventricular end diastolic volume and stroke volume.  Comparison of right atrial pressure (CVP) to CO is indirect and insensitive estimate of the relationship.
2. Initial CVP is sometimes high even with significant volume deficit, especially in patient with COPD, generalised vasoconstriction and rapid fluid replacement.  May also be high due use of vasopressors or PASG.
3. A minimal rise in initial low CVP with fluid therapy suggests need for further volume expansion.
4. A declining CVP suggests ongoing fluid loss.
5. An abrupt or persistent elevation in CVP suggests volume replacement is adequate, too rapid or cardiac function is compromised.
6. Pronounced elevation of the CVP may be caused by hypervolaemia, cardiac dysfunction, cardiac tamponade or increased intrathoracic pressure from a pneumothorax.  Think also catheter malposition.

• Ideal position for line is in superior vena cava, just proximal to the right atrium.
• Complications of CVP lines are infections, vascular injury, nerve injury, embolisation, thrombosis and pneumothorax.
• CVP represents right heart function and may not be representative of left heart function in patient with 1° myocardial dysfunction or abnormal pulmonary circulation.

C. Recognition of other problems.

When patient fails to respond to fluid therapy consider:

1. Cardiac tamponade.
2. Tension pneumothorax.
3. Ventilatory problems.
4. Unrecognised fluid loss.
5. Acute gastric distension.
6. Myocardial infarction.
7. Diabetic acidosis.
8. Hypoadrenalism.

Final Summary

• Constant reevaluation, ESPECIALLY WHEN PATIENT DEVIATES FROM EXPECTED PATTERNS IS KEY TO TREATMENT.
• Consider surgey in all patients who have profound hypovolemic shock
• REMEMBER VASOPRESSORS ARE CONTRAINDICATED IN TREATMENT OF HYPOVOLAEMIC SHOCK.
• Remember that ultimately the goal is to restore perfusion of organs and optimise oxygen delivery