SHOCK
CVS Monitoring and Shock
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?
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 body’s response
to cellular metabolic insufficiency”
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
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
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 <65%)
or central venous oxygen saturation (SCVO2 <70%)
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
.
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
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
Effects of Sympatho-adrenal response
Organ
Effect
Eye
Dilates pupil
Heart
Increases rate and force of contraction
Lungs
Dilates bronchioles
Digestive tract
Inhibits peristalsis
Kidney
Increases renin secretion
Skin
Cold, sweating
Penis
Promotes ejaculation (!)
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.”
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
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
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)
Distributive Shock

associated with severely decreased SVR leading
to intravascular volume deficit
•
•
•
•
sepsis
anaphylaxis
spinal cord injury
vasodilatory drugs
Cardiogenic Shock

Reduced contractility
•
•
•
•
acute LVF
myocardial infarction
arrhythmias
cardiomyopathy
Obstructive Shock

Impediment to forward flow:
• tension pneumothorax
• pulmonary embolus
• cardiac tamponade
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 A&E.
- 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
Areas of circulatory support
Circulatory support involves manipulation of the main
determinants of Cardiac Output:
1.
Preload via volume replacement
2.
Myocardial contractility via inotropic agents
3.
Afterload via vasoactive agents
1:Preload and volume replacement
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
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)
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)
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 Hb>7g/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)
Fluid requirements in illness
Table: Contents of common crystalloids in mmol/L
Plasma
Na Cl 0.9%
Dextrose 5%
Dextrose Saline
(4%/0.18%)
Hartmann’s solution
Lactated Ringer’s sol’n
Na
K
Ca
Cl
140
4.3
2.3
100
26
154
0
0
154
0
308
5.0
0
0
0
0
0
278
4.0
30
0
0
0
0
283
4.0
131
5.0
2.0
111
0
275
6.5
Lactate
29
2.2
109
0
273
6.9
130
4.0
Lactate
HCO3
Osmolality
pH
285-300
7.4
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
The volume of fluid (water) within a
compartment is determined by its membrane
properties and solute concentrations
TBW = 60% of body weight in male, 50-55% in female
ECF – 40% of TBW
ICF – 60% of TBW
Na + 140
K +4
Cl – 105
HCO3 - 28
20% Intra vascular
fluids
Vascular endothelium
As a result of a
membrane-bound
ATP-dependent pump
ex-changes Na for K+
potassium is the most
important de-terminant of
intracellular osmotic
pressure
Cell membrane
K + 100, Na + 10
Interstitial
Plasma proteins (albumin)
80%
Intracellular fluids
!<------------------------------------------------------------------------------------------------------------------------ 5% Dextrose/Dextrose Saline
!<------------------------------------------------ 0.9% Na Cl / Ringer’s Lactate
!<------------------- Colloids
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
For the first 10 kg
For the next 10-20 kg
For each kg above 20kg
RATE
100 ml/kg/24hrs
or
4 ml/kg/hr
Add 50 ml/kg/24hrs
or
+2 ml/kg/hr
Add 20 ml/kg/24hrs
or
+1 ml/kg/hr
So, the maintenance fluid requirement for a 25kg child is:
1000 + 500 + 100 = 1600 (ml/24hrs)
or 40 + 20 + 5 = 65 (ml/hr)
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
Replacement
Predictable fluid losses
Increased insensible losses
hyperventilation, fever and sweating (extra 500ml/day is required for
every degree Celsius above 37°C)
“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)
Some examples of predictable losses
Redistributive and evaporative perioperative surgical losses
Degree of Tissue Trauma
Additional Fluid requirement
Minimal (eg herniorrhapy)
Moderate (eg cholecystectomy)
Severe (eg bowel resection)
0-2 ml/kg/hr (25ml/kg/day)
2-4 ml/kg/hr (>50ml/kg/day)
4-8 ml/kg/hr (>100ml/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
- Add colloids after 24 hrs
GIFTASUP 2008
GIFTASUP recommendations
Number
Recommendation
Evidence
level
1
Don’t use ‘Normal Saline’
1b
2
Don’t use Dextrose/D. Saline
1b
3
For maintenance, use low Na+, high K+
8
‘Normal saline’ for hypochloraemia
Replace stomach losses with potassium in a crystalloid
Replace bowel losses with balanced crystalloid
9
Use ‘Goal-directed therapy’
1b
10
Use invasive monitoring, preferably ‘Flow-based’
If unavailable, clinical and laboratory measurements
1b
11
Treat blood loss with blood; treat hypovolaemia with
crystalloid or colloid
1b
12
If diagnosis of hypovolaemia in doubt, fluid challenge
1b
5
2,5,5
2: Contractility and Inotropic agents
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.
Choice of Drugs
Inotropes
• Predominant Beta effect (Direct or Indirect)
Vasopressors
• Predominant Alpha Agonists
• Vasopressin
Vasodilators
• Nitrates
• Some Beta-2 Agonists
• Phosphodiesterase Inhibitors (Inodilators)
2. Contractility and Inotropic agents
Inotropes:
Direct predominant action on β receptors:
• Adrenaline (via CVP line only)
• Dobutamine (might reduce SVR)
• Dopamine (cardiac versus renal doses)
Pure Beta agonists:
• Dopexamine (β1 » β2)
• Isoprenaline (β1 > β2)
Indirect acting:
• Ephedrine
3: Afterload and Vasoactive drugs
3. Afterload: Vasopressors
Alpha agonist with some beta effects:
• Noradrenaline
the most potent (via CVP line only)
Synthetic Alpha agonists:
• Metaraminol
• Phenylephrine
• Methoxamine
can all be given peripherally
Others
• Ephedrine
• Vasopressin
indirect Alpha and Beta effect
if patient not responding to Noradrenaline
3. Afterload: Vasodilators
• Nitrates:
GTN (Glyceryl Trinitrate)
Sodium nitroprusside
donate nitrosyl group aka nitric oxide
• Beta Agonists:
Dopexamine
Isoprenaline
increased cardiac output
causes reflex vasodilation
• Phosphodiesterase inhibitors:
Milrinone
Enoximone
decrease SVR plus
positive inotropic effect
Properties of commonly used inotropic
and vasopressor agents
Beta-1
Beta-2
Alpha-1
Alpha-2 DA-1
DA-2
Adrenaline:
Low dose
++
+
+
+
N/A
N/A
High dose
+++
+++
++++
+++
N/A
N/A
++
0
+++
+++
N/A
N/A
Dobutamine
++++
+
+
0
0
0
Dopexamine
+
+++
0
0
++
+
Low dose
+
0
+
+
++
+
High dose
+++
++
++
+
++
+
Noradrenaline
Dopamine:
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
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?
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.
Case 1

Treatment of CVS failure:
•
•
•
•
IV fluid boluses 1l Hartmann’s 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 Cryst:Colloid ratio 3:1
• 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.
Cardiogenic shock
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
Management
Diagnosis
• Hx IHD, chest pain, ECG,
• troponin, enzymes
Treatment
• Supportive measures
Oxygenation, filling, cardiac support
• Thrombolysis
• Angiography
- PTCA and stenting
Case 2

A 55-year-old man is on the coronary care unit
when he develops a low urine output (<0.5 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 37°C.
He had an inferolateral myocardial infarction 24
hours ago. The nurse is concerned about his
urine output.
How do you assess his volume status?
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.
Obstructive shock
• Tension pneumothorax
• Cardiac tamponade
• Pulmonary embolism
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
Cardiac tamponade
Heart cannot fill, so (again) features of shock with high CVP
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
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
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?
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.
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)
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 < 70%)
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
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.
Central Venous Catheterisation
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
Arterial Cannulation Sites
Site
Advantages
Disadvantages
Radial artery
Easy to palpate
Well tolerated
Low risk of ischemia due to ulnar
artery collaterals
Contraindicated in hand
ischemia
High risk of thrombosis
Interferes with the wrist
movement
Brachial
artery
Easy to palpate
Ischemia after thrombosis can
have serious implications
Interferes with arm movement
Femoral
artery
Easy to palpate
Low risk of thrombosis due to high
collateral flow
Most accurately reflects aortic
pressure
Interferes with flexion of hip
Vicinity of highly contaminated
perineum
Easily palpable and imaged
May be absent
Contraindicated in foot
ischemia
Dorsalis Pedis
artery
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 (ABG’s, U&E’S, glucose etc)
-Patient with physiological difficulties for NIBP (obesity, AF)
SV max
-------------------------------------------------SVV
-------------------------------------------------SV min
Stroke volume variation (SVV) :
difference between the highest and the
lowest arterial wave traces during
respiratory cycle
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
Oesophageal Doppler
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)
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.
Questions