SHOCK - PowerPoint PPT Presentation


PPT – SHOCK PowerPoint presentation | free to download - id: 3d0689-YzZhN


The Adobe Flash plugin is needed to view this content

Get the plugin now

View by Category
About This Presentation



Lecture for Warwick Medical Students ... CVS Monitoring and Shock * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * Techniques to ... – PowerPoint PPT presentation

Number of Views:120
Avg rating:3.0/5.0
Slides: 73
Provided by: mededcove
Learn more at:
Tags: shock


Write a Comment
User Comments (0)
Transcript and Presenter's Notes

Title: 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
  • Q 2. Do you think this patient is in some kind of

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

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
    lt65) or central venous oxygen saturation (SCVO2

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
  • 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
  • Venoconstriction increases cardiac
  • Arteriolar constriction maintains blood
  • 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
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
Types of shock
  • Shock with low CVP
  • Hypovolaemic shock - lack of circulating blood
  • Distributive shock - abnormal peripheral
  • 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
  • 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
  • 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
  • - 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
  • 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
  • Preload via volume replacement
  • Myocardial contractility via inotropic agents
  • Afterload via vasoactive agents

  • 1Preload 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
  • Con volume expansion transient (half-life
    20-30 min) fluid accumulates in interstitial
  • pulmonary oedema may result
  • (initial resuscitation 20 ml/kg bolus over 30
  • 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

Fluid requirements in illness
  • Blood and blood products
  • Pro clearly indicated in haemorrhagic shock
  • maintain Hb concentration at an acceptable
  • 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
  • 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)

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
  • 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
  • Na Bicarbonate 8.4 1000 0 0 0 1000 2000

(No Transcript)
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
  • 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

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

  • 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)

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
  • Moderate (eg cholecystectomy) 2-4 ml/kg/hr
  • Severe (eg bowel resection) 4-8 ml/kg/hr
  • 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
  • Fluid to use - Use predominantly crystalloid
    in the first 12-24 hrs

GIFTASUP recommendations
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 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

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

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

Properties of commonly used inotropic and
vasopressor agents

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
  • Q 2. Do you think this patient is in some kind of

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
  • 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 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
  • If becomes hypotensive despite fluid
    resuscitation consider invasive monitoring and
    vasopressors or inotropic drugs via central line

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

  • 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 (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
  • 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

(No Transcript)
Tension pneumothorax
  • Valve mechanism air into pleural space but not
  • 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
  • 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
  • Echocardiography may help, exploration is
  • 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
  • Diagnose with invasive pulmonary angiography or
  • Supportive treatment oxygen, filling, cardiac
  • 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
  • When direct flow measurements are not possible
    fluid challenges should be given and the response

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

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)

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
Direct arterial pressure monitoring
  • Invasive cannulation of an artery for continuous
    monitoring of direct BP used in
  • Haemodynamically unstable patient, patient in
  • 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

SV min
Techniques to assess cardiac output (Flow based
  • 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

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
  • Afterload or SVR - by calculating from the
  • SVR CO / MAP

(No Transcript)
(No Transcript)
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
  • It was uncertain if PAC guided therapy improved
    outcome in patients with septic shock.