SHOCK

1
SHOCK

• CVS Monitoring and Shock

2
Case 1

• A 40 year old man comes to the ED having fallen
  on the path and hurt his left lower ribs. His
  observations are
• pulse 110 bpm
• blood pressure 140/90 mmHg
• You notice how clammy he feels to touch.
• Q 1. Could this man have a life-threatening
  haemorrhage?
• Q 2. Do you think this patient is in some kind of
  shock?

3
Definitions of shock

• An acute circulatory failure with inadequate or
  inappropriately distributed tissue perfusion
  resulting in generalised cellular hypoxia and
  global hypoperfusion.
• A situation when the intravascular space is
  larger than the existing intravascular volume
  volume deficit
• A complex clinical syndrome that is the bodys
  response to cellular metabolic insufficiency

4
Global hypoperfusion

• Clinical assessment
• Peripheries
• Evaluate skin colour and temperature
• Sweating
• Pulse volume
• Capillary refill
• Skin turgor
• Level of consciousness
• as indicator of the cerebral perfusion

5
Global hypoperfusion

• Measurement
• Vital signs
• Heart rate
• Blood pressure
• Respiratory rate
• Pulse oximetry
• Urine output (a measure of renal perfusion)
• NB some patients will maintain a normal blood
  pressure, despite hypovolaemia as a result of
  massive catecholamine release

6
Global hypoperfusion

• Laboratory
• compromised tissue perfusion leads to cellular
  hypoxia, anaerobic glycolysis and production of
  lactic acid, resulting in
• Metabolic acidosis (Base deficit)
• Low pH
• Raised blood lactate level (above 2.0 mmol/l)
• Reduced mixed venous oxygen saturation (SvO2
  lt65) or central venous oxygen saturation (SCVO2
  lt70)

7
Host responses

• Microcirculatory changes
• Early
• blood / fluid returns to circulation due to
  increased sympathetic tone and autoregulation
  (sympatho-adrenal response)
• mobilization of interstitial fluid
• Late
• tissue damage promotes release of inflammatory
  mediators
• complement, cytokines, platelet activating
  factor, products of arachidonic acid
  metabolism, lysosomal enzymes
• inappropriate vasodilatation
• capillary permeability increases (capillary leak
  syndrome) causing
• hypotension
• Increased viscosity
• intravascular coagulation
• .

8
Effects of Sympatho-adrenal response

• Immediate
• Increased contractility and heart rate to
  support cardiac output in patient with moderate
  hypovolaemia
• Venoconstriction increases cardiac
  filling
• Arteriolar constriction maintains blood
  pressure
• Blood flow re-distributed (centralisation) to
  vital organs brain,
  heart, kidneys, liver, respiratory muscles

9
Effects of Sympatho-adrenal response

• Delayed
• Kidney reduced filtration and increased
  re-absorption restores circulating volume via
  Renin-Angiotensin-Aldosterone System
• Capillary reduced hydrostatic pressure
  leads to fluid moving from ECF to intravascular
  space, causing haemodilution and volume expansion

10
Effects of Sympatho-adrenal response
11
Could be irreversible!
If abnormalities of tissue perfusion are allowed
to persist, the function of vital organs will be
impaired (from compensated to uncompensated and
finally irreversible phases).

• In the 1940s, Carl Wiggers simulated haemorrhagic
  shock in dogs and developed an animal model of
  'irreversible shock' in which all animals would
  die despite aggressive resuscitation.

Shock is a syndrome resulting from a depression
of many functions but in which reduction of
effective circulating volume and pressure are of
basic importance and in which impairment of the
circulation steadily progresses until it
eventuates in a state of irreversible circulatory
failure.
12
Types of shock

• Shock with low CVP
• Hypovolaemic shock - lack of circulating blood
  volume
• Distributive shock - abnormal peripheral
  microcirculation
• Shock with raised CVP
• Cardiogenic shock - pump failure
• Obstructive shock - mechanical impediment to
  forward flow

13
Hypovolaemic Shock

• Exogenous losses
• haemorrhage
• diarrhoea and vomiting
• burns
• Endogenous losses
• into the surrounding tissues or into the body
  cavities
• intestinal obstruction
• occult haemorrhage
• ascites

14
Hypovolaemic Shock

• Clinical signs reflecting intravascular volume
  deficit include
• Capillary refill, pulse volume and heart rate
• Jugular (central) venous pressure (JVP/CVP)
• Oliguria - urine output less than 0.5ml/kg/hr for
  2 consecutive hours / less than 400ml per 24
  hours
• Urine output should be interpreted in the light
  of all other clinical signs
• Trend in arterial pulse waves (increased Stroke
  Volume Variability - SVV)

15
Distributive Shock

• associated with severely decreased SVR leading to
  intravascular volume deficit
• sepsis
• anaphylaxis
• spinal cord injury
• vasodilatory drugs

16
Cardiogenic Shock

• Reduced contractility
• acute LVF
• myocardial infarction
• arrhythmias
• cardiomyopathy

17
Obstructive Shock

• Impediment to forward flow
• tension pneumothorax
• pulmonary embolus
• cardiac tamponade

18
Management of shock

• A-B-C
• OXYGEN THERAPY
• VENTILATORY SUPPORT
• HAEMODYNAMIC SUPPORT
• MONITOR AND CLOSE OBSERVATION
• - BP, HR, SpO2, resp. rate every ½-1 hr
  depending on situation,
• - Fluid balance - input/output hourly,
• - Consider invasive monitoring early in AE.
• - Temperature,
• - GCS when indicated
• TIME-SENSITIVE CARE
• Correct the underlying cause
• e.g. - surgical intervention to stop haemorrhage,
  treat ileus or diarrhoea, identify fluid losses,
  treat infection and sepsis

19
Areas of circulatory support

• Circulatory support involves manipulation of the
  main determinants of Cardiac Output
• Preload via volume replacement
• Myocardial contractility via inotropic agents
• Afterload via vasoactive agents

20

• 1Preload and volume replacement

21
General principles

• The appropriate rate of fluid administration
  should be guided by clinical reassessment and
  sensible limits
• Choose the type of fluid which will best treat
  the deficit or maintain euvolaemia
• Where a fluid deficit is identified (e.g.
  haemorrhage, diarrhoea, vomiting, insensible or
  renal losses), the nature (content) of this
  deficit should be identified
• Goal Directed Therapy - implementation of the
  proposed clinical endpoints and monitoring of
  fluid status

22
Initial fluid resuscitation strategy

• Dehydration vs. Shock
• Dehydration does not cause death, but shock does.
• Dehydration includes significant depletion of all
  fluid compartments in the body and may eventually
  lead to shock
• The treatment of dehydration requires gradual
  replacement of fluids, with electrolyte content
  similar to the specific losses
• The treatment of shock requires rapid restoration
  of intravascular volume by giving fluid that
  approximates plasma electrolyte content (bolus 20
  ml/kg over 30 min)

23
Fluid requirements in illness

• Crystalloids
• Pro cheap, convenient to use, free of side
  effects
• Con volume expansion transient (half-life
  20-30 min) fluid accumulates in interstitial
  space
• pulmonary oedema may result
• (initial resuscitation 20 ml/kg bolus over 30
  min)
• Colloids (starch - Volulyte, gelatin - Isoplex)
• Pro greater increase in plasma volume
• more sustained (half-life 3-6 hrs)
• Con cost
• allergic reactions
• clotting abnormalities
• (initial resuscitation 0.2-0.3g/kg bolus over 30
  min)

24
Fluid requirements in illness

• Blood and blood products
• Pro clearly indicated in haemorrhagic shock
• maintain Hb concentration at an acceptable
  level
• Con cost
• risk (small, but significant consequences)
• (keep Hbgt7g/dl unless patient has ischaemic heart
  disease, then 10g/dl)
• Albumin
• Pro similar to colloid in terms of long
  half-life
• possibly some benefit from transport function
  of albumin
• Con cost
• (should be used only in special circumstances -
  for example burns, cirrhotic liver disease and
  children with septic shock)

25
Table Contents of common crystalloids in mmol/L
Fluid requirements in illness

• Na K Ca Cl HCO3
  Osmolality pH
• Plasma 140 4.3 2.3 100 26 285-300 7.4
• Na Cl 0.9 154 0 0 154 0 308 5.0
• Dextrose 5 0 0 0 0 0 278 4.0
• Dextrose Saline (4/0.18) 30 0 0 0
  0 283 4.0
• Hartmanns solution 131 5.0 2.0 111 0 275
  6.5
• Lactate 29
• Lactated Ringers soln 130 4.0 2.2 109 0
  273 6.9
• Lactate 28
• Na Bicarbonate 1.2 150 0 0 0 150 300
  8.0
• Na Bicarbonate 8.4 1000 0 0 0 1000 2000
  8.0

26
(No Transcript)
27
Fluid requirements in illness

• Goals of fluid therapy may be
• Resuscitation restoration of intravascular volume
• Replacement of deficit and ongoing losses
• Maintenance alone
• Maintenance - Normal requirements could be
  estimated from table
• WEIGHT RATE
• For the first 10 kg 100
  ml/kg/24hrs or 4 ml/kg/hr
• For the next 10-20 kg Add 50
  ml/kg/24hrs or 2 ml/kg/hr
• For each kg above 20kg Add 20 ml/kg/24hrs
  or 1 ml/kg/hr
• So, the maintenance fluid requirement for a 25kg
  child is

28
Replacement

• Overt losses
• Loss of fluid to the exterior
• bleeding, vomiting, excessive diuresis or
  diarrhoea
• Occult losses
• Fluid sequestration in body cavities or tissues
• obstructed bowel, ascites, intramuscular
  haematoma

29
Replacement

• Predictable fluid losses
• Increased insensible losses
• hyperventilation, fever and sweating (extra
  500ml/day is required for every degree Celsius
  above 37C)
• Capillary leak syndrome
• characterized by prolonged and severe increase
  in capillary permeability as a result of
  hypoalbuminaemia, septicemia and toxins
• Evaporative losses
• due to large wounds or burns directly
  proportional to the surface area exposed and/or
  the duration of the surgical procedure
• Third spacing
• internal redistribution of fluids within soft
  tissues massive fluid shifts (tissue swelling in
  peritonitis, pancreatitis, other infection sites)
  

30
Some examples of predictable losses

• Redistributive and evaporative perioperative
  surgical losses
• Degree of Tissue Trauma Additional
  Fluid requirement
• Minimal (eg herniorrhapy) 0-2 ml/kg/hr
  (25ml/kg/day)
• Moderate (eg cholecystectomy) 2-4 ml/kg/hr
  (gt50ml/kg/day)
• Severe (eg bowel resection) 4-8 ml/kg/hr
  (gt100ml/kg/day)
• PARKLANDS FORMULA for patient with severe burns
• 4ml x body weight (kg) x burns ml/day
• Regime - 1st 8 hours ½ the calculated volume
• - Next 16 hours remaining ½ calculated
  volume
• Fluid to use - Use predominantly crystalloid
  in the first 12-24 hrs

31
GIFTASUP 2008
32
GIFTASUP recommendations
33
2 Contractility and Inotropic agents
34
General principles

• If signs of shock persist despite volume
  replacement, inotropic or other vasoactive agents
  may be given to improve blood pressure and
  cardiac output.
• The effects of a particular drug in an individual
  patient are unpredictable and the response must
  be closely monitored.
• An invasive monitoring (CVP line, arterial line)
  is mandatory for most of the cases
• All drugs have very short biological half lives
  (1-2 min). Steady state concentration achieved in
  5-10 min from the beginning of IV infusion
• Effects are associated with an increased
  myocardial oxygen consumption and could be
  damaging to the myocardium.

35
Choice of Drugs

• Inotropes
• Predominant Beta effect (Direct or Indirect)
• Vasopressors
• Predominant Alpha Agonists
• Vasopressin
• Vasodilators
• Nitrates
• Some Beta-2 Agonists
• Phosphodiesterase Inhibitors (Inodilators)

36
2. Contractility and Inotropic agents

• Inotropes
• Direct predominant action on ß receptors
• Adrenaline (via CVP line only)
• Dobutamine (might reduce SVR)
• Dopamine (cardiac versus renal doses)
• Pure Beta agonists
• Dopexamine (ß1 ß2)
• Isoprenaline (ß1 gt ß2)
• Indirect acting
• Ephedrine

37
3 Afterload and Vasoactive drugs
38
3. Afterload Vasopressors

• Alpha agonist with some beta effects
• Noradrenaline the most potent (via CVP line
  only)
• Synthetic Alpha agonists
• Metaraminol
• Phenylephrine can all be given peripherally
• Methoxamine
• Others
• Ephedrine indirect Alpha and Beta effect
• Vasopressin if patient not responding to
  Noradrenaline

39
3. Afterload Vasodilators

• Nitrates
• GTN (Glyceryl Trinitrate) donate nitrosyl group
  -
• Sodium nitroprusside aka nitric oxide
• Beta Agonists
• Dopexamine increased cardiac output
• Isoprenaline causes reflex vasodilation
• Phosphodiesterase inhibitors
• Milrinone decrease SVR plus
• Enoximone positive inotropic effect

40
Properties of commonly used inotropic and
vasopressor agents

41
Summary of circulatory support

• First priority is to secure the Airway and, if
  necessary, provide mechanical ventilation (B)
• Adequate volume replacement is essential in all
  cases (C)
• In patients with continued evidence of impaired
  tissue oxygenation moderate doses of inotropes
  may be given to further increase oxygen delivery.
• Tissue perfusion must be restored by maintaining
  an adequate cardiac output and systemic blood
  pressure with reference to premorbid values

42
Case 1

• A 40 year old man comes to the ED having fallen
  on the path and hurt his left lower ribs. His
  observations are
• pulse 110 bpm
• blood pressure 140/90 mmHg
• You notice how clammy he feels to touch.
• Q 1. Could this man have a life-threatening
  haemorrhage?
• Q 2. Do you think this patient is in some kind of
  shock?

43
Case 1

• Yes. It is highly possible that this man has
  ruptured his spleen.
• He could have lost 20-30 of his circulating
  blood volume already and needs urgent fluid
  resuscitation, imaging and surgery.
• Immediate management A-B-C.
• A -Airway is okay.
• B - Check breathing (for pneumothorax) and
  insert two large bore cannulae for fluid.
• C - Circulation is assessed by looking at the
  vital signs and for signs of hypoperfusion
  (for example, skin temperature, capillary
  refill).
• This patient has cold peripheries and is
  tachycardic but not hypotensive.
• A 40-year-old man with a severe bleed may
  compensate by vasoconstriction.

44
Case 1

• Treatment of CVS failure
• IV fluid boluses 1l Hartmanns over 30 min.
• Blood given to maintain Hb above 7.5
• Regular reassessment of all parameters
• Repeated fluid boluses including blood products
  colloids and crystalloids with CrystColloid
  ratio 31
• Definitive treatment surgical with or without
  imaging
• If becomes hypotensive despite fluid
  resuscitation consider invasive monitoring and
  vasopressors or inotropic drugs via central line
  catheter.

45
Cardiogenic shock
46
Cardiogenic shock

• Reduced contractility (usually) due to ischaemia
  and infarction of myocardium
• Features of shock
• High LVEDP
• Low CO
• Pulmonary congestion
• Shock with high CVP

47
Management

• Diagnosis
• Hx IHD, chest pain, ECG,
• troponin, enzymes
• Treatment
• Supportive measures
• Oxygenation, filling, cardiac support
• Thrombolysis
• Angiography
• - PTCA and stenting

48
Case 2

• A 55-year-old man is on the coronary care unit
  when he develops a low urine output (lt0.5 ml/kg
  per hour for the last 2 hours). He has cool hands
  and feet. His vital signs
• pulse 90bpm,
• blood pressure 110/50 mmHg,
• respiratory rate 22 per minute,
• core temperature 37C.
• He had an inferolateral myocardial infarction 24
  hours ago. The nurse is concerned about his urine
  output.
• How do you assess his volume status?

49
Case 2

• Patients admitted to hospital following a
  myocardial infarction can be dehydrated due to
  vomiting, sweating, and reduced oral intake.
• In this case, you would want to know if there are
  any crackles audible in the lungs. Arterial blood
  gases may reveal a base deficit.
• A fluid challenge can be given safely if there
  are signs of hypovolaemia or if there is any
  uncertainty about this patient's volume status.
• The definition of cardiogenic shock includes a
  low cardiac output state, which is unresponsive
  to fluid and this implies that fluid is still
  used in the assessment of this condition.

50
Obstructive shock

• Tension pneumothorax
• Cardiac tamponade
• Pulmonary embolism

51
(No Transcript)
52
Tension pneumothorax

• Valve mechanism air into pleural space but not
  out
• Increasing pressure collapses lung, then pushes
  mediastinum and heart to other side
• Raised intrathoracic pressure and kinked great
  veins prevent cardiac filling
• Features of shock with high central venous
  pressure
• Diagnosis
• Often young patient with history of sudden
  shortness of breath, possibly associated with
  trauma or asthma
• Examination of the affected side shows poor
  expansion, absent breath sounds and tympanic
  percussion note trachea and apex beat are
  shifted to opposite side
• Treatment
• immediate decompression with needle then chest
  drain with underwater seal

53
Cardiac tamponade
Heart cannot fill, so (again) features of shock
with high CVP
54
Cardiac tamponade

• Diagnosis
• History of trauma or cardiac surgery, myocardial
  infarction, uraemia, anticoagulation.
• May be difficult to distinguish from cardiogenic
  shock
• Echocardiography may help, exploration is
  definitive
• Treatment
• Supportive measures
• Oxygen, filling, cardiac support.
• Sub-xiphoid pericardiocentesis, ideally with
  fluoroscopic control
• Surgical exploration

55
Pulmonary embolism

• Large clot in pulmonary artery causes acute
  overloading of RV and hypovolaemia of LA and LV
• Features of shock with high CVP
• Crushing central chest pain
• Evidence of DVT may be present
• May look very similar to cardiogenic shock
• ECG may help SI QIII TIII (only in 30 of
  cases)
• Diagnose with invasive pulmonary angiography or
  CTPA
• Supportive treatment oxygen, filling, cardiac
  support
• After resuscitation - anticoagulation,
  thrombolysis, surgery

56
Case 3

• An 80-year-old lady is admitted with abdominal
  pain and malaena. She has a permanent pacemaker
  and is treated for congestive cardiac failure,
  which is under control. Her pulse and blood
  pressure are normal.
• Q. How can you assess her volume status?

57
Case 3

• The elderly do not respond physiologically to
  bleeding in the same way as younger patients.
• The history of a gastrointestinal bleed points to
  volume depletion, as does chronic diuretic use.
• Although she has a "normal" blood pressure - is
  it normal for her?
• Special attention must be paid to other markers
  of hypoperfusion in this lady, as pulse and blood
  pressure (including orthostatic measurements)
  will be of little value.
• Look at peripheral skin temperature and
  respiratory rate, and perform an arterial blood
  gas analysis.
• A urinary catheter should be inserted to monitor
  hourly urine output.
• In this case volume status can be incredibly
  difficult to assess without using flow based
  techniques.
• When direct flow measurements are not possible
  fluid challenges should be given and the response
  assessed.

58
CVS Monitoring

• Non-invasive techniques
• Clinical assessment of tissue perfusion
• ECG, NiBP, pulse oximetry
• Non-invasive CO studies Echo, PiCCO, NiCO
  method
• Invasive Monitoring
• Central venous pressure monitoring
• Direct arterial line pressure monitoring
• Cardiac Output studies (Pulmonary Artery
  Catheter)

59
Clinical assessment of tissue perfusion

• Peripheries
• evaluate skin colour and temperature
• capillary refill, skin turgor, pulse volume
• Level of consciousness
• as indicator of the cerebral perfusion
• Urine output
• as indicator of the renal perfusion pressure
• oliguria due to renal conservation
• Metabolic insufficiency
• acidaemia (Base deficit)
• Raised blood lactate (above 2.0 mmol/L)
• Reduced mixed venous O2 saturation (SCVO2 lt 70)

60
Assessment of intravascular volume

• Clinical signs reflecting intravascular volume
  deficit include
• Capillary refill, pulse volume, heart rate
• Jugular (central) venous pressure (JVP / CVP)
• Trend in arterial pulse waves (increased SVV)
• Urine output should be interpreted in the light
  of these clinical signs
• output less than 0.5ml/kg per hour for 2
  consecutive hours or
• less than 400ml per 24 hours
• nb not blood pressure

61
Central Venous Catheterisation

• Internal jugular vein
• Subclavian vein
• Axillary vein
• Femoral vein
• The absolute value is often unhelpful, except in
  extreme cases of severe hypovolaemia, significant
  fluid overload, or heart failure.
• Correct interpretation requires assessment of the
  change in central venous pressure in response to
  a fluid challenge in conjunction with alterations
  in other monitored variables.

62
Central Venous Catheterisation
63
Complications of central catheters

• On insertion
• Cardiac arrythmias
• Pneumothorax / haemothorax
• Air embolism
• Surrounding tissue injuries
• Cardiac tamponade
• Post insertion
• Infection (consider removal after 7 days)
• Cardiac arrhythmias
• Displacement of catheter
• Blockage of lumen(s)
• Air / material embolism
• Thrombus formation

64
Arterial Cannulation Sites
65
Direct arterial pressure monitoring

• Invasive cannulation of an artery for continuous
  monitoring of direct BP used in
• Haemodynamically unstable patient, patient in
  shock
• Patient receiving inotropic / vasoactive agents
• For blood sampling (ABGs, UES, glucose etc)
• Patient with physiological difficulties for NIBP
  (obesity, AF)

SV max
--------------------------------------------------
Stroke volume variation (SVV) difference
between the highest and the lowest arterial wave
traces during respiratory cycle
SVV
--------------------------------------------------

SV min
66
Techniques to assess cardiac output (Flow based
techniques)

• Oesophageal Doppler
• based on determination of RBC velocity
• Transoesophageal Echocardiography
• Gold standard in US
• Arterial pulse wave analysis
• eg PiCCO, Vigileo, LiDCO
• Partial CO2 rebreathing technique
• based on exhaled CO2 measurement (capnography) eg
  NiCO

67
Oesophageal Doppler
68
Pulmonary artery catheterisation

• Dr. Jeremy Swan and Dr. William Ganz
• Developed 1971
• Catheterisation of the pulmonary artery with a
  balloon flotation catheter allows to measure
• Preload - indirect assessment of the filling
  pressure of the left ventricle (pulmonary artery
  occlusion or wedge pressure)
• Contractility by using thermodilution
  technique
• Afterload or SVR - by calculating from the
  formula
• SVR CO / MAP
• (PAC PAFC PAOP PAWP)

69
(No Transcript)
70
(No Transcript)
71
Pulmonary artery catheter controversy

• PAC-Man study (Lancet, 2005)
• 1,041 patients, randomized to PAC or no PAC
• PAC guided therapy altered diagnosis and improved
  functional outcome in the traumatically injured
  patient, but the effect on mortality was
  uncertain.
• It was uncertain if PAC guided therapy improved
  outcome in patients with septic shock.

72
Questions