SHOCK

SHOCKSHOCK

CVS Monitoring and ShockCVS Monitoring and Shock

Case 1Case 1

A A 40 year old man comes to the ED having fallen on the 40 year old man comes to the ED having fallen on the path and hurt his left lower ribs. His observations are: path and hurt his left lower ribs. His observations are:

pulse 110 bpmpulse 110 bpm blood pressure 140/90 mmHgblood pressure 140/90 mmHg

You notice how clammy he feels to touch. You notice how clammy he feels to touch.

Q 1.Q 1. Could this man have a life‑threatening Could this man have a life‑threatening haemorrhage? haemorrhage?

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

Definitions of shock: Definitions of shock:

““An acute circulatory failure with inadequate or An acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in inappropriately distributed tissue perfusion resulting in

generalised cellular hypoxia and generalised cellular hypoxia and global global hypoperfusionhypoperfusion.” .”

““A situation when the intravascular space is larger than A situation when the intravascular space is larger than the existing intravascular volume – the existing intravascular volume – volume deficitvolume deficit ” ”

““A complex clinical syndrome that isA complex clinical syndrome that is the body’sthe body’s responseresponse to to cellularcellular metabolic insufficiency metabolic insufficiency””

Global hypoperfusionGlobal hypoperfusion

Clinical assessment:Clinical assessment:

Peripheries:Peripheries:• Evaluate skin colour and temperatureEvaluate skin colour and temperature• SweatingSweating• Pulse volumePulse volume• Capillary refillCapillary refill• Skin turgorSkin turgor

Level of consciousness:Level of consciousness:• as indicator of the cerebral perfusionas indicator of the cerebral perfusion

Global hypoperfusionGlobal hypoperfusion

Measurement:Measurement:

Vital signsVital signs:: Heart rateHeart rate Blood pressure*Blood pressure* Respiratory rateRespiratory rate Pulse oximetryPulse oximetry Urine output (a measure of renal perfusion)Urine output (a measure of renal perfusion)

*NB: some patients will maintain a normal blood pressure, despite *NB: some patients will maintain a normal blood pressure, despite hypovolaemia as a result of massive catecholamine releasehypovolaemia as a result of massive catecholamine release

Global hypoperfusionGlobal hypoperfusionLaboratoryLaboratory::

compromised tissue perfusion leads to cellular hypoxia, compromised tissue perfusion leads to cellular hypoxia, anaerobic glycolysis and production of lactic acid, anaerobic glycolysis and production of lactic acid, resulting in:resulting in:

Metabolic acidosis (Metabolic acidosis (Base deficitBase deficit)) Low pHLow pH Raised blood Raised blood llactate level (above 2.0 mmol/l)actate level (above 2.0 mmol/l) Reduced mixed venous oxygen saturation (SReduced mixed venous oxygen saturation (SvvOO22

<65%) or central venous oxygen saturation (S<65%) or central venous oxygen saturation (SCVCVOO22 <70%)<70%)

Host responses 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 responseEffects of Sympatho-adrenal response

Immediate:

• Increased contractility and heart rateto support cardiac output in patient with moderate hypovolaemia

• Venoconstriction increases cardiac filling

• Arteriolar constrictionmaintains blood pressure

• Blood flow re-distributed (centralisation) to vital organs brain, heart, kidneys, liver, respiratory muscles

Effects of Sympatho-adrenal responseEffects 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 responseEffects of Sympatho-adrenal response

OrganOrgan EffectEffect

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!Could be irreversible!

In the 1940s, Carl Wiggers simulated haemorrhagic shock in dogs In the 1940s, Carl Wiggers simulated haemorrhagic shock in dogs and developed an animal model of 'and developed an animal model of 'irreversibleirreversible shockshock' in ' in

which all animals would die despite aggressive resuscitation.which all animals would die despite aggressive resuscitation.

If abnormalities of tissue perfusion are allowed to If abnormalities of tissue perfusion are allowed to persist, the function of vital organs will be impaired persist, the function of vital organs will be impaired (from compensated to uncompensated and finally (from compensated to uncompensated and finally

irreversible phases).irreversible phases).

“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 shockTypes of shock

Shock with low CVP:Shock with low CVP:Hypovolaemic shock - lack of circulating blood volume

Distributive shock - abnormal peripheral microcirculation

Shock with raised CVP:Shock with raised CVP:Cardiogenic shock - “pump failure”

Obstructive shock - mechanical impediment to forward flow

Hypovolaemic ShockHypovolaemic Shock

• Exogenous lossesExogenous losses haemorrhagehaemorrhage diarrhoea and vomitingdiarrhoea and vomiting burnsburns

• Endogenous lossesEndogenous losses into the surrounding tissues or into the body cavitiesinto the surrounding tissues or into the body cavities

• intestinal obstructionintestinal obstruction• occult haemorrhageoccult haemorrhage• ascitesascites

Hypovolaemic ShockHypovolaemic Shock

Clinical signs reflecting Clinical signs reflecting intravascular volume intravascular volume deficitdeficit include: include:

• Capillary refill, pCapillary refill, pulse volume and heart rateulse volume and heart rate• Jugular (central) venous pressure (JVP/CVP)Jugular (central) venous pressure (JVP/CVP)• Oliguria - uOliguria - urine outputrine output less than 0.5ml/kg/hr less than 0.5ml/kg/hr for 2 for 2

consecutive hours /consecutive hours / less than 400ml per 24 hours less than 400ml per 24 hours Urine output should be interpreted in the light of Urine output should be interpreted in the light of

all other clinical signsall other clinical signs• Trend in arterial pulse waves (increased Stroke Trend in arterial pulse waves (increased Stroke

Volume Variability - SVV)Volume Variability - SVV)

Distributive ShockDistributive Shock

associated with severely decreased SVR leading associated with severely decreased SVR leading to intravascular volume deficit to intravascular volume deficit

• sepsissepsis• anaphylaxisanaphylaxis• spinal cord injuryspinal cord injury• vasodilatory drugsvasodilatory drugs

Cardiogenic ShockCardiogenic Shock

Reduced contractilityReduced contractility

• acute LVFacute LVF• myocardial infarctionmyocardial infarction• arrhythmiasarrhythmias• cardiomyopathycardiomyopathy

Obstructive ShockObstructive Shock

Impediment to forward flow:Impediment to forward flow:

• tension pneumothoraxtension pneumothorax• pulmonary emboluspulmonary embolus• cardiac tamponadecardiac tamponade

Management of shockManagement 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 Correct the underlying cause

•e.g. - surgical intervention to stop haemorrhage, treat ileus or e.g. - surgical intervention to stop haemorrhage, treat ileus or diarrhoeadiarrhoea, identify fluid losses, treat infection and sepsis, identify fluid losses, treat infection and sepsis

Areas of circulatory supportAreas of circulatory support

Circulatory support involves manipulation of the main Circulatory support involves manipulation of the main determinants of Cardiac Output:determinants of Cardiac Output:

1.1. PreloadPreload via volume replacementvia volume replacement

2.2. Myocardial contractilityMyocardial contractility via ivia inotropic notropic agentsagents

3.3. AfterloadAfterload via vasoactive agentsvia vasoactive agents

1:Preload and volume replacement1:Preload and volume replacement

General principlesGeneral 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 Initial fluid resuscitation strategy

Dehydration vs. ShockDehydration vs. Shock

Dehydration does not cause death, but Dehydration does not cause death, but shock doesshock does..

Dehydration includes significant depletion of Dehydration includes significant depletion of allall fluid fluid compartments in the body and compartments in the body and may eventuallymay eventually lead to shock lead to shock

The treatment of dehydration requires The treatment of dehydration requires gradual gradual replacement of replacement of fluids, with electrolyte content similar to the specific lossesfluids, with electrolyte content similar to the specific losses

The treatment of The treatment of shockshock requires requires rapidrapid restoration of restoration of intravascular volume by giving fluid that approximates plasma intravascular volume by giving fluid that approximates plasma electrolyte content electrolyte content ((bolus 20 ml/kg over 30 minbolus 20 ml/kg over 30 min))

Fluid requirements in illnessFluid requirements in illnessCrystalloids:Crystalloids:

Pro:Pro: cheap, convenient to use, free of side effectscheap, convenient to use, free of side effects

Con: Con: volume expansion transient (half-life 20-30 min) volume expansion transient (half-life 20-30 min) fluid accumulates in interstitial spacefluid accumulates in interstitial space

pulmonary oedema may resultpulmonary oedema may result ((initial resuscitation: 20 ml/kg bolus over 30 mininitial resuscitation: 20 ml/kg bolus over 30 min))

Colloids:Colloids: (starch - Volulyte, gelatin - Isoplex) (starch - Volulyte, gelatin - Isoplex)

Pro:Pro: greater increase in plasma volumegreater increase in plasma volume

more sustained (half-life 3-6 hrs) more sustained (half-life 3-6 hrs)

Con:Con: costcost

allergic reactionsallergic reactions

clotting abnormalities clotting abnormalities ((initial resuscitation: 0.2-0.3g/kg bolus over 30 mininitial resuscitation: 0.2-0.3g/kg bolus over 30 min))

Fluid requirements in illnessFluid requirements in illnessBlood Blood andand blood products: blood products:

Pro:Pro: clearly indicated in haemorrhagic shockclearly indicated in haemorrhagic shock

maintain Hb concentration at an acceptable level*maintain Hb concentration at an acceptable level*

Con:Con: costcost

risk (small, but significant consequences)risk (small, but significant consequences)(keep Hb>7g/dl unless patient has ischaemic heart disease, then 10g/dl)(keep Hb>7g/dl unless patient has ischaemic heart disease, then 10g/dl)

AlbuminAlbumin Pro:Pro: similar to colloid in terms of long half-lifesimilar to colloid in terms of long half-life

possibly some benefit from transport function of possibly some benefit from transport function of albuminalbumin

Con:Con: costcost

((should be used only in special circumstances - for example: burns, cirrhotic liver should be used only in special circumstances - for example: burns, cirrhotic liver disease and children with septic shock)disease and children with septic shock)

Table: Contents of common crystalloids in mmol/LTable: Contents of common crystalloids in mmol/L

NaNa K K Ca Ca Cl HCO3 Osmolality pH Cl HCO3 Osmolality pH

PlasmaPlasma 140140 4.34.3 2.32.3 100100 26 285-300 7.426 285-300 7.4

Na Cl 0.9%Na Cl 0.9% 154 154 0 0 0 0 154154 0 0 308 308 5.05.0

Dextrose 5%Dextrose 5% 0 0 0 0 0 0 0 0 0 0 278 278 4.0 4.0

Dextrose Saline Dextrose Saline (4%/0.18%)(4%/0.18%) 3030 0 0 0 0 0 0 00 283 283 4.0 4.0

Hartmann’s solutionHartmann’s solution 131 131 5.05.0 2.02.0 111111 0 0 275 6.5 275 6.5

Lactate 29 Lactate 29

Lactated Ringer’sLactated Ringer’s sol’nsol’n 130 130 4.04.0 2.22.2 109109 0 0 273 6.9 273 6.9

Lactate 28Lactate 28

Na Bicarbonate 1.2%Na Bicarbonate 1.2% 150 150 0 0 0 0 0 0 150 150 300 300 8.0 8.0

Na Bicarbonate 8.4%Na Bicarbonate 8.4% 10001000 0 0 0 0 0 0 10001000 20002000 8.0 8.0

Fluid requirements in illnessFluid requirements in illness

The volume of fluid (water) within a The volume of fluid (water) within a compartment is determined by its membrane compartment is determined by its membrane

properties and solute concentrationsproperties and solute concentrations

Intracellular fluids

K + 100, Na + 10As a result of amembrane-bound

ATP-dependent pump ex changes Na for K+

potassium is the most important de terminant of

intracellular osmotic pressure

ICF – 60% of TBW

TBW = 60% of body weight in male, 50-55% in female

ECF – 40% of TBW

80%

Interstitial

fluids

Na + 140

K + 4

Cl – 105

HCO3 - 28

20%

Intra

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Cell m

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!<------------------------------------------------------------------------------------------------------------------------ 5% Dextrose/Dextrose Saline!<------------------------------------------------ 0.9% Na Cl / Ringer’s Lactate

!<------------------- Colloids

Fluid requirements in illnessFluid requirements in illness

Goals of fluid therapy may be:Goals of fluid therapy may be:• ResuscitationResuscitation restoration of intravascular volume restoration of intravascular volume• Replacement Replacement of deficit and ongoing lossesof deficit and ongoing losses• MaintenanceMaintenance alone alone

MaintenanceMaintenance - Normal requirements could be estimated from table:- Normal requirements could be estimated from table:

WEIGHTWEIGHT RATERATEFor the first 10 kg For the first 10 kg 100 ml/kg/24hrs100 ml/kg/24hrs oror 4 ml/kg/hr 4 ml/kg/hrFor the next 10-20 kg For the next 10-20 kg Add 50 ml/kg/24hrsAdd 50 ml/kg/24hrs or +or +2 ml/kg/hr 2 ml/kg/hr For each kg above 20kg For each kg above 20kg Add 20 ml/kg/24hrsAdd 20 ml/kg/24hrs oror +1 ml/kg/hr +1 ml/kg/hr

So, the maintenance fluid requirement for a 25kgSo, the maintenance fluid requirement for a 25kg child is:child is:1000 + 500 + 100 = 1600 (ml/24hrs) 1000 + 500 + 100 = 1600 (ml/24hrs)

or 40 + 20 + 5 = 65 (ml/hr)or 40 + 20 + 5 = 65 (ml/hr)

ReplacementReplacement

Overt lossesOvert losses

Loss of fluid to the exteriorLoss of fluid to the exteriorbleeding, vomiting, bleeding, vomiting, excessive excessive diuresis or diarrhoeadiuresis or diarrhoea

Occult lossesOccult losses

Fluid sequestration Fluid sequestration in body cavities orin body cavities or tissues tissuesobstructed bowel,obstructed bowel, ascites ascites, intramuscular haematoma, intramuscular haematoma

ReplacementReplacement

Predictable fluid lossesPredictable fluid losses

Increased insensible lossesIncreased insensible losseshyperventilation, fever and sweating (hyperventilation, fever and sweating (extra 500ml/day is required for extra 500ml/day is required for every degree Celsius above 37°C)every degree Celsius above 37°C)

““Capillary leak syndrome”Capillary leak syndrome”characterized by prolonged and severe increase in capillary characterized by prolonged and severe increase in capillary permeability as a result of hypoalbuminaemia, septicemia and toxinspermeability as a result of hypoalbuminaemia, septicemia and toxins

EvaporativeEvaporative losses lossesdue to large wounds or burns; directly proportional to the surface area due to large wounds or burns; directly proportional to the surface area exposed and/or the duration of the surgical procedure exposed and/or the duration of the surgical procedure

““Third Third sspacing“pacing“ internal redistribution of fluids within soft tissues; massive fluid shifts internal redistribution of fluids within soft tissues; massive fluid shifts (tissue swelling in peritonitis, pancreatitis, other infection sites)(tissue swelling in peritonitis, pancreatitis, other infection sites)

Some examples of predictable lossesSome examples of predictable losses

Redistributive and evaporative perioperative surgical lossesRedistributive and evaporative perioperative surgical losses

Degree of Tissue Trauma Degree of Tissue Trauma Additional Fluid requirementAdditional Fluid requirement

Minimal (eg herniorrhapy)Minimal (eg herniorrhapy) 0-2 ml/kg/hr (25ml/kg/day)0-2 ml/kg/hr (25ml/kg/day)Moderate (eg cholecystectomy)Moderate (eg cholecystectomy) 2-4 ml/kg/hr (>50ml/kg/day)2-4 ml/kg/hr (>50ml/kg/day)Severe (eg bowel resection)Severe (eg bowel resection) 4-8 ml/kg/hr (>100ml/kg/day)4-8 ml/kg/hr (>100ml/kg/day)

PARKLANDS FORMULA for patient with severe burns:PARKLANDS FORMULA for patient with severe burns:

4ml x body weight (kg) x % burns = ml/day4ml x body weight (kg) x % burns = ml/day

Regime: Regime: -- 11stst 8 hours: ½ the calculated volume 8 hours: ½ the calculated volume- Next 16 hours: remaining ½ calculated volume- Next 16 hours: remaining ½ calculated volume

Fluid to useFluid to use:: -- Use predominantly crystalloid in the first 12-24 hrsUse predominantly crystalloid in the first 12-24 hrs-- Add colloids after 24 hrsAdd colloids after 24 hrs

GIFTASUP 2008GIFTASUP 2008

GIFTASUP recommendationsGIFTASUP recommendations

Number RecommendationEvidence

level

1 Don’t use ‘Normal Saline’ 1b

2 Don’t use Dextrose/D. Saline 1b

3 For maintenance, use low Na+, high K+ 5

8

‘Normal saline’ for hypochloraemiaReplace stomach losses with potassium in a crystalloidReplace bowel losses with balanced crystalloid

2,5,5

9 Use ‘Goal-directed therapy’ 1b

10Use invasive monitoring, preferably ‘Flow-based’If unavailable, clinical and laboratory measurements

1b

11Treat blood loss with blood; treat hypovolaemia with crystalloid or colloid

1b

12 If diagnosis of hypovolaemia in doubt, fluid challenge 1b

2:2: ContractilityContractility and and Inotropic Inotropic agentsagents

General principlesGeneral principles

If signs of shock persist despite volume replacement, If signs of shock persist despite volume replacement, inotropic or inotropic or other vasoactiveother vasoactive agents may be given to improve blood pressure agents may be given to improve blood pressure and cardiac output. and cardiac output.

The effects of a particular drug in an individual patient are The effects of a particular drug in an individual patient are unpredictable and the response must be closely monitored. unpredictable and the response must be closely monitored.

An An invasive monitoringinvasive monitoring (CVP line, arterial line) is mandatory for most (CVP line, arterial line) is mandatory for most of the casesof the cases

All drugs have very short biological half lives (1-2 min). Steady state All drugs have very short biological half lives (1-2 min). Steady state concentration achieved in 5-10 min from the beginning of IV infusionconcentration achieved in 5-10 min from the beginning of IV infusion

Effects are associated with aEffects are associated with ann increased myocardial oxygen increased myocardial oxygen consumption and could be damaging to the myocardiumconsumption and could be damaging to the myocardium..

Choice of DrugsChoice of Drugs

InotropesInotropes• Predominant Predominant Beta effect (Beta effect (DirectDirect or or IndirectIndirect))

VasopressorsVasopressors• Predominant Alpha AgonistsPredominant Alpha Agonists• VasopressinVasopressin

VasodilatorsVasodilators• NitratesNitrates• Some Some Beta-2 Agonists Beta-2 Agonists • Phosphodiesterase Inhibitors (Inodilators) Phosphodiesterase Inhibitors (Inodilators)

2. Contractility2. Contractility and and Inotropic Inotropic agentsagents

Inotropes:Inotropes: Direct predominant action on Direct predominant action on ββ receptors receptors::• Adrenaline (via CVP line only)Adrenaline (via CVP line only)• Dobutamine (might reduce SVR)Dobutamine (might reduce SVR)• Dopamine (cardiac versus renal doseDopamine (cardiac versus renal doses)s)

Pure Beta agonistsPure Beta agonists::• Dopexamine (Dopexamine (ββ11 » » ββ22))• Isoprenaline (Isoprenaline (ββ1 1 > > ββ22))

Indirect actingIndirect acting: : • EphedrinEphedrinee

3: Afterload and Vasoactive drugs3: Afterload and Vasoactive drugs

3. Afterload:3. Afterload: VasopressorsVasopressors

Alpha agonist with some beta effects:Alpha agonist with some beta effects:• NoradrenalineNoradrenaline the most potent (via CVP line only)the most potent (via CVP line only)

Synthetic Alpha agonists:Synthetic Alpha agonists:• MetaraminolMetaraminol• Phenylephrine Phenylephrine can all be given peripherallycan all be given peripherally

• MethoxamineMethoxamine

OthersOthers• Ephedrine Ephedrine indirect Alpha and Beta effectindirect Alpha and Beta effect

• VasopressinVasopressin if patient not responding to if patient not responding to NoradrenalineNoradrenaline

3. Afterload:3. Afterload: VasodilatorsVasodilators

• Nitrates: Nitrates: GTN (Glyceryl Trinitrate)GTN (Glyceryl Trinitrate) donate nitrosyl group -donate nitrosyl group -

Sodium nitroprussideSodium nitroprusside aka nitric oxideaka nitric oxide

• Beta Agonists:Beta Agonists:DopexamineDopexamine increased cardiac outputincreased cardiac output

IsoprenalineIsoprenaline causes reflex vasodilationcauses reflex vasodilation

• Phosphodiesterase inhibitors:Phosphodiesterase inhibitors: MMiilrinonelrinone decrease SVR plusdecrease SVR plus

EnoximoneEnoximone positive inotropic effectpositive inotropic effect

Properties of commonly usedProperties of commonly used inotropic inotropic and vasopressor and vasopressor agentsagents

Beta-1Beta-1 Beta-2Beta-2 Alpha-1Alpha-1 Alpha-2Alpha-2 DA-1DA-1 DA-2DA-2

Adrenaline:Adrenaline:

Low doseLow dose ++++ ++ ++ ++ N/AN/A N/AN/A

High doseHigh dose ++++++ ++++++ ++++++++ ++++++ N/AN/A N/AN/A

NoradrenalineNoradrenaline ++++ 00 ++++++ ++++++ N/AN/A N/AN/A

DobutamineDobutamine ++++++++ ++ ++ 00 00 00DopexamineDopexamine ++ ++++++ 00 00 ++++ ++

Dopamine:Dopamine:

Low doseLow dose ++ 00 ++ ++ ++++ ++

High doseHigh dose ++++++ ++++ ++++ ++ ++++ ++

Summary of circulatory supportSummary of circulatory support

First priority is to secure the First priority is to secure the AAirway and, if necessary, irway and, if necessary, provide mechanical ventilation (provide mechanical ventilation (BB))

Adequate volume replacement is essential in all cases (Adequate volume replacement is essential in all cases (CC))

In patients with continued evidence of impaired tissue In patients with continued evidence of impaired tissue oxygenation moderate doses of oxygenation moderate doses of inotropesinotropes may be given to may be given to further increase oxygen delivery.further increase oxygen delivery.

Tissue perfusion must be restored by maintaining an Tissue perfusion must be restored by maintaining an adequate cardiac output and systemic blood pressure with adequate cardiac output and systemic blood pressure with reference to premorbid valuesreference to premorbid values

Case 1Case 1

A A 40 year old man comes to the ED having fallen on the 40 year old man comes to the ED having fallen on the path and hurt his left lower ribs. His observations are: path and hurt his left lower ribs. His observations are:

pulse 110 bpmpulse 110 bpm blood pressure 140/90 mmHgblood pressure 140/90 mmHg

You notice how clammy he feels to touch. You notice how clammy he feels to touch.

Q 1.Q 1. Could this man have a life‑threatening Could this man have a life‑threatening haemorrhage? haemorrhage?

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

Case 1Case 1YesYes. It is highly possible that this man has ruptured his spleen. . It is highly possible that this man has ruptured his spleen.

He could have lost 20‑30% of his circulating blood volume already He could have lost 20‑30% of his circulating blood volume already and needs urgent fluid resuscitation, imaging and surgery.and needs urgent fluid resuscitation, imaging and surgery.

Immediate management: Immediate management: A-B-C. A-B-C. A -Airway is okay. A -Airway is okay.

B - Check breathing (for pneumothorax) and insert two B - Check breathing (for pneumothorax) and insert two large bore cannulae for fluid. large bore cannulae for fluid.

C - Circulation is assessed by looking at the vital signs C - Circulation is assessed by looking at the vital signs and for signs of hypoperfusion (for example, skin and for signs of hypoperfusion (for example, skin temperature, capillary refill). temperature, capillary refill).

This patient has cold peripheries and is tachycardic but not This patient has cold peripheries and is tachycardic but not hypotensive.hypotensive.

A 40‑year‑old man with a severe bleed may compensate by A 40‑year‑old man with a severe bleed may compensate by vasoconstriction.vasoconstriction.

Case 1Case 1

Treatment of CVS failure: Treatment of CVS failure: • IV fluid boluses 1l Hartmann’s over 30 min.IV fluid boluses 1l Hartmann’s over 30 min.• Blood given to maintain Hb above 7.5Blood given to maintain Hb above 7.5• Regular reassessment of all parametersRegular reassessment of all parameters• Repeated fluid boluses including blood products colloids Repeated fluid boluses including blood products colloids

and crystalloids with Cryst:Colloid ratio 3:1and crystalloids with Cryst:Colloid ratio 3:1• Definitive treatment – surgical with or without imagingDefinitive treatment – surgical with or without imaging• If becomes hypotensive despite fluid resuscitation If becomes hypotensive despite fluid resuscitation

consider invasive monitoring and vasopressors or consider invasive monitoring and vasopressors or inotropic drugs via central line catheter.inotropic drugs via central line catheter.

Cardiogenic shockCardiogenic shock

Cardiogenic shockCardiogenic shock

Reduced contractility (usually) due to Reduced contractility (usually) due to ischaemia and infarction of myocardiumischaemia and infarction of myocardium

• Features of shock:Features of shock: High LVEDPHigh LVEDP Low COLow CO Pulmonary congestionPulmonary congestion

Shock with high Shock with high CVPCVP

ManagementManagement

DiagnosisDiagnosis• Hx IHD, chest pain, ECG, Hx IHD, chest pain, ECG, • troponin, enzymestroponin, enzymes

TreatmentTreatment• Supportive measuresSupportive measures

Oxygenation, filling, cardiac supportOxygenation, filling, cardiac support

• ThrombolysisThrombolysis• AngiographyAngiography

- PTCA and stenting- PTCA and stenting

Case 2Case 2 A 55‑year‑old man is on the coronary care unit A 55‑year‑old man is on the coronary care unit

when he develops a low urine output (<0.5 ml/kg when he develops a low urine output (<0.5 ml/kg per hour for the last 2 hours). He has cool hands per hour for the last 2 hours). He has cool hands and feet. His vital signs: and feet. His vital signs: • pulse 90bpm, pulse 90bpm, • blood pressure 110/50 mmHg, blood pressure 110/50 mmHg, • respiratory rate 22 per minute, respiratory rate 22 per minute, • core temperature 37°C. core temperature 37°C.

He had an inferolateral myocardial infarction 24 He had an inferolateral myocardial infarction 24 hours ago. The nurse is concerned about his hours ago. The nurse is concerned about his urine output.urine output.

How do you assess his volume status? How do you assess his volume status?

Case 2Case 2 Patients admitted to hospital following a myocardial infarction Patients admitted to hospital following a myocardial infarction

can be dehydrated due to vomiting, sweating, and reduced oral can be dehydrated due to vomiting, sweating, and reduced oral intake. intake.

In this case, you would want to know if there are any crackles In this case, you would want to know if there are any crackles audible in the lungs. Arterial blood gases may reveal a base audible in the lungs. Arterial blood gases may reveal a base deficit. deficit.

A fluid challenge can be given safely if there are signs of A fluid challenge can be given safely if there are signs of hypovolaemia or if there is any uncertainty about this patient's hypovolaemia or if there is any uncertainty about this patient's volume status. volume status.

The definition of cardiogenic shock includes a low cardiac output The definition of cardiogenic shock includes a low cardiac output state, which is unresponsive to fluid and this implies that fluid is state, which is unresponsive to fluid and this implies that fluid is still used in the assessment of this condition.still used in the assessment of this condition.

Obstructive shockObstructive shock

• Tension pneumothoraxTension pneumothorax• Cardiac tamponadeCardiac tamponade• Pulmonary embolismPulmonary embolism

Tension pneumothoraxTension pneumothorax

Valve mechanism: air into pleural space but not outValve mechanism: air into pleural space but not out Increasing pressure collapses lung, then pushes mediastinum Increasing pressure collapses lung, then pushes mediastinum

and heart to other sideand heart to other side Raised intrathoracic pressure and kinked great veins prevent Raised intrathoracic pressure and kinked great veins prevent

cardiac fillingcardiac filling Features of shock with high central venous pressureFeatures of shock with high central venous pressure

Diagnosis Diagnosis Often Often young patientyoung patient with history of sudden shortness of breath, with history of sudden shortness of breath,

possibly associated with trauma or asthmapossibly associated with trauma or asthma Examination of the affected side shows poor expansion, absent Examination of the affected side shows poor expansion, absent

breath sounds and tympanic percussion note; trachea and apex breath sounds and tympanic percussion note; trachea and apex beat are shifted to opposite sidebeat are shifted to opposite side

Treatment Treatment immediate decompression with needle then chest drain with immediate decompression with needle then chest drain with

underwater seal underwater seal

Cardiac tamponadeCardiac tamponade

Heart cannot fill, so (again) features of shock with high CVP

Cardiac tamponadeCardiac tamponade

DiagnosisDiagnosis• History of trauma or cardiac surgery, myocardial History of trauma or cardiac surgery, myocardial

infarction, uraemia, anticoagulation.infarction, uraemia, anticoagulation.• May be difficult to distinguish from cardiogenic shockMay be difficult to distinguish from cardiogenic shock• Echocardiography may help, exploration is definitiveEchocardiography may help, exploration is definitive

TreatmentTreatment• Supportive measuresSupportive measures

Oxygen, filling, cardiac support.Oxygen, filling, cardiac support.• Sub-xiphoid pericardiocentesis, ideally with Sub-xiphoid pericardiocentesis, ideally with

fluoroscopic controlfluoroscopic control• Surgical explorationSurgical exploration

Pulmonary embolismPulmonary embolism

• Large clot in pulmonary artery causes acute overloading of Large clot in pulmonary artery causes acute overloading of RV and hypovolaemia of LA and LVRV and hypovolaemia of LA and LV

• Features of shock with Features of shock with high high CVPCVP• Crushing central chest painCrushing central chest pain• Evidence of DVT may be presentEvidence of DVT may be present• May look very similar to cardiogenic shockMay look very similar to cardiogenic shock

• ECG may help – SECG may help – SII Q QIIIIII T TIIIIII (only in 30% of cases) (only in 30% of cases)

• Diagnose with invasive pulmonary angiography or CTPADiagnose with invasive pulmonary angiography or CTPA• Supportive treatment : oxygen, filling, cardiac supportSupportive treatment : oxygen, filling, cardiac support• After After resuscitationresuscitation - a - anticoagulation, thrombolysis, surgerynticoagulation, thrombolysis, surgery

Case 3Case 3

An 80‑year‑old lady is admitted with abdominal An 80‑year‑old lady is admitted with abdominal pain and malaena. She has a permanent pain and malaena. She has a permanent pacemaker and is treated for congestive cardiac pacemaker and is treated for congestive cardiac failure, which is under control. Her pulse and failure, which is under control. Her pulse and blood pressure are normal. blood pressure are normal.

Q. How can you assess her volume status?Q. How can you assess her volume status?

Case 3Case 3The elderly do not respond physiologically to bleeding in the same way as The elderly do not respond physiologically to bleeding in the same way as

younger patients. younger patients.

• The history of a gastrointestinal bleed points to volume depletion, as does chronic diuretic use. 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?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 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. blood pressure (including orthostatic measurements) will be of little value.

• Look at peripheral skin temperature and respiratory rate, and perform an arterial blood gas Look at peripheral skin temperature and respiratory rate, and perform an arterial blood gas analysis. analysis.

• A urinary catheter should be inserted to monitor hourly urine output. 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 In this case volume status can be incredibly difficult to assess without using flow based techniques. based techniques.

When direct flow measurements are not possible When direct flow measurements are not possible fluid challenges should be fluid challenges should be given and the response assessedgiven and the response assessed. .

CVS MonitoringCVS Monitoring

Non-invasive techniques: Non-invasive techniques: • Clinical assessment of tissue perfusion Clinical assessment of tissue perfusion • ECG, NiBP, pulseECG, NiBP, pulse oximetry; oximetry; • Non-invasive CO studies – Echo, PiCCO, NiCO methodNon-invasive CO studies – Echo, PiCCO, NiCO method

Invasive Monitoring:Invasive Monitoring:• Central venous pressure monitoring; Central venous pressure monitoring; • Direct arterial line pressure monitoring;Direct arterial line pressure monitoring;• Cardiac Output studies (Pulmonary Artery Catheter)Cardiac Output studies (Pulmonary Artery Catheter)

Clinical assessment of tissue Clinical assessment of tissue perfusion:perfusion:

Peripheries:Peripheries:• evaluate skin colour and temperatureevaluate skin colour and temperature• capillary refill, skin turgorcapillary refill, skin turgor, p, pulse volume ulse volume

Level of consciousness:Level of consciousness:• as indicator of the cerebral perfusionas indicator of the cerebral perfusion

Urine output:Urine output:• as indicator of the renal perfusion pressure as indicator of the renal perfusion pressure • oliguria – due to renal conservationoliguria – due to renal conservation

Metabolic insufficiency: Metabolic insufficiency: • acidaemia (acidaemia (Base deficitBase deficit))• Raised blood Raised blood llactate (above 2.0 mmol/L)actate (above 2.0 mmol/L)

• Reduced mixed venous O2 saturation (SReduced mixed venous O2 saturation (SCVCVO2 < 70%)O2 < 70%)

Assessment of intravascular volumeAssessment of intravascular volume

Clinical signs reflecting Clinical signs reflecting intravascular volume deficitintravascular volume deficit include: include:

• Capillary refill, pCapillary refill, pulse volume, heart rateulse volume, heart rate• Jugular (central) venous pressure (JVP / CVP)Jugular (central) venous pressure (JVP / CVP)• Trend in arterial pulse waves (increased SVV) Trend in arterial pulse waves (increased SVV) • Urine output should be interpreted in the light of these Urine output should be interpreted in the light of these

clinical signs clinical signs outputoutput less than 0.5ml/kg per less than 0.5ml/kg per hour for 2 hour for 2 consecutiveconsecutive hours hours oror less than 400ml per 24 hoursless than 400ml per 24 hours

nb: nb: not blood pressurenot blood pressure

Central Venous CatheterisationCentral Venous Catheterisation

Internal jugular veinInternal jugular vein Subclavian veinSubclavian vein Axillary veinAxillary vein Femoral veinFemoral vein

TThe he absolute valueabsolute value is often unhelpful, except in extreme is often unhelpful, except in extreme cases of severe hypovolaemia, significant fluid overload, or cases of severe hypovolaemia, significant fluid overload, or heart failure.heart failure.

Correct interpretation requires assessment of the Correct interpretation requires assessment of the change in change in central venous pressurecentral venous pressure in response to a in response to a fluid challengefluid challenge in conjunction with alterations in other monitored variables.in conjunction with alterations in other monitored variables.

Central Venous CatheterisationCentral Venous Catheterisation

Complications of central cathetersComplications of central catheters

• On insertionOn insertion Cardiac arrythmiasCardiac arrythmias Pneumothorax / haemothoraxPneumothorax / haemothorax Air embolismAir embolism Surrounding tissue injuries Surrounding tissue injuries Cardiac tamponadeCardiac tamponade

• Post insertionPost insertion Infection (consider removal after 7 days)Infection (consider removal after 7 days) Cardiac arrhythmiasCardiac arrhythmias Displacement of catheterDisplacement of catheter Blockage of lumen(s)Blockage of lumen(s) Air / material embolismAir / material embolism Thrombus formationThrombus formation

Arterial Cannulation SitesArterial Cannulation Sites

SiteSite AdvantagesAdvantages DisadvantagesDisadvantages

Radial arteryRadial artery

Easy to palpateEasy to palpate

Well toleratedWell tolerated

Low risk of ischemia due to ulnar Low risk of ischemia due to ulnar artery collateralsartery collaterals

Contraindicated in hand Contraindicated in hand ischemiaischemia

High risk of thrombosisHigh risk of thrombosis

Interferes with the wrist Interferes with the wrist movementmovement

BrachialBrachial

arteryarteryEasy to palpateEasy to palpate

Ischemia after thrombosis can Ischemia after thrombosis can have serious implications have serious implications

Interferes with arm movementInterferes with arm movement

Femoral Femoral artery artery

Easy to palpateEasy to palpate

Low risk of thrombosis due to high Low risk of thrombosis due to high collateral flowcollateral flow

Most accurately reflects aortic Most accurately reflects aortic pressurepressure

Interferes with flexion of hipInterferes with flexion of hip

Vicinity of highly contaminated Vicinity of highly contaminated perineumperineum

Dorsalis Pedis Dorsalis Pedis arteryartery Easily palpable and imagedEasily palpable and imaged

May be absentMay be absent

Contraindicated in foot Contraindicated in foot ischemiaischemia

Direct arterial pressure monitoringDirect arterial pressure monitoring

Invasive cannulation of an artery for continuousInvasive cannulation of an artery for continuous monitoring of direct BP; used in:monitoring of direct BP; used in:

-Haemodynamically unstable patient, patient in shockHaemodynamically unstable patient, patient in shock-Patient receiving inotropic Patient receiving inotropic / vasoactive / vasoactive agentsagents-For blood sampling (ABG’s, U&E’S, glucose etc)For blood sampling (ABG’s, U&E’S, glucose etc)-Patient with physiological difficulties for NIBP (obesity, AF)Patient with physiological difficulties for NIBP (obesity, AF)

SV max

SV min

--------------------------------------------------

-------------------------------------------------- Stroke volume variationStroke volume variation (SVV) :

difference between the highest and the lowest arterial wave traces during

respiratory cycle

SVV

TTechniques echniques toto assess cardiac assess cardiac output output (Flow based techniques)(Flow based techniques)

Oesophageal DopplerOesophageal Doppler• based on determination of RBC velocitybased on determination of RBC velocity

TTransoesophageal Echocardiographyransoesophageal Echocardiography• Gold standard Gold standard iin USn US

Arterial pArterial pulse wave ulse wave analysisanalysis• eg Pieg PiCCO, Vigileo, LiDCOCCO, Vigileo, LiDCO

Partial CO2 rebreathing techniquePartial CO2 rebreathing technique• based on exhaled CObased on exhaled CO22 measurement (capnography) eg NiCO measurement (capnography) eg NiCO

Oesophageal DopplerOesophageal Doppler

Pulmonary artery catheterisationPulmonary artery catheterisation

Dr. Jeremy Dr. Jeremy SwanSwan and Dr. William and Dr. William GanzGanz Developed 1971 Developed 1971 Catheterisation of the pulmonary artery with a balloon flotation Catheterisation of the pulmonary artery with a balloon flotation

catheter allows to measure:catheter allows to measure:

• PPreload - indirect assessment of the filling pressure of the left reload - indirect assessment of the filling pressure of the left ventricle (pulmonary artery occlusion or wedge pressure)ventricle (pulmonary artery occlusion or wedge pressure)

• Contractility – by using ‘thermodilution’ techniqueContractility – by using ‘thermodilution’ technique

• Afterload or SVR - by calculating from the formulaAfterload or SVR - by calculating from the formulaSVR = CO / MAPSVR = CO / MAP

(PAC; PAFC; PAOP; PAWP)(PAC; PAFC; PAOP; PAWP)

Pulmonary artery catheter controversy Pulmonary artery catheter controversy

PAC-Man study (Lancet, 2005)PAC-Man study (Lancet, 2005)

1,041 patients, randomized to PAC or no PAC1,041 patients, randomized to PAC or no PAC

PAC guided therapy altered diagnosis and improved PAC guided therapy altered diagnosis and improved functional outcome in the traumatically injured patient, but functional outcome in the traumatically injured patient, but the effect on mortality was uncertain.the effect on mortality was uncertain.

It was uncertain if PAC guided therapy improved outcome in It was uncertain if PAC guided therapy improved outcome in patients with septic shock.patients with septic shock.

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