Circulatory failure in Intensive Care
Dr….
Circulatory System
• Ensures adequate blood flow to supply
metabolic demands of the tissues
• Regulation via cardiac pump and peripheral
vascular system
• Pump control varies the cardiac output
• PVS control regulates intravascular volume,
vascular resistance, perfusion pressure and
appropriately distributes flows to vascular
beds
Circulatory failure = shock
‘Tissue perfusion is inadequate
for the metabolic needs of the
patient’
Inadequate O2 delivery
• Inadequate O2 delivery represents an imbalance of
delivery relative to need
• This imbalance between supply and demand leads to
the development of tissue hypoxia
• Changes in systemic perfusion are always present in
shock
Classification of Shock
• Cardiogenic
– Infarction/ischaemic VSD/myocarditis
– Valvular abnormalities/PE/Tamponade
• Hypovolaemic
– Haemorrhage
– Excessive fluid loss from GI/Renal tracts/Burns
• Septic
• Neurogenic
• Anaphylactic
Oxygen delivery (DO2)
• Amount of O2 delivered to peripheral tissues
• Dependent on arterial O2 content and cardiac output
• In health this is about 1005ml/min
• DO2 is reduced in cardiogenic and hypovolaemic shock
(impaired contractility and reduced myocardial preload
respectively)
Oxygen Transport
Oxygen
transport
DO2 =
Cardiac
output
SaO2 x 1.34
Arterial
oxygen
saturation
x [Hba] x CO
Arterial
haemoglobin
concentration
Oxygen content of
1g fully saturated
haemoglobin
Arterial Oxygen Content
Oxygen uptake (VO2)
• Amount of O2 taken up by the tissues
• It is the difference between DO2 and O2 returned to
lung in mixed venous blood
• In health this is about 760 ml/min
• An oxygen debt occurs when uptake exceeds delivery
(as occurs in shock) and severity can be monitored by
rising blood lactate (anaerobic metabolism)
Septic Shock
• Soluble cell bound receptors recognize microbial
components or their toxins and stimulate release of
pro-inflammatory and anti-inflammatory cytokines,
complement, coagulation activation and platelet
aggregation.
• This results in vasodilatation and reduced intravascular volume (due increased vascular
permeability)
• Despite reduced contractility cardiac output is often
increased in septic shock due to reduced afterload
Septic Shock
• Initially DO2 is elevated in septic shock primarily
due to increased CO
• However, VO2 is also raised due to increased
metabolic activity of the tissues
• When VO2 exceeds DO2 a lactic acidosis results
• Untreated this leads to multi-organ failure
Clinical presentation of septic
shock
• Hyperdynamic (unless significant hypovolaemia)
• Proven source of infection
• Hypotension
• Signs of systemic inflammation (tachycardia,
tachypnoea, hypo/perthermia, leuko-cytosis/paenia)
• Confused, tachycardic, tachypnoeic, oliguric
• Bounding pulses and warm peripheries
Hypovolaemic and cardiogenic shock
• Low cardiac output
• BP can initially be normal due to compensatory
sympathetic and neuro-hormonal mechanisms
• Patients will be confused, pale, tachycardic,
tachypnoeic, poor perfusion and oliguric
• CVP low in HV shock
• CVP high in CG shock with associated pulmonary
oedema
Investigations
• Tailor to history and clinical findings.
• FBC, Clotting, Electrolytes, Cr, Ur, Clotting,
CRP, ABGs, lactate, troponin and blood
cultures.
• ECG, CXR.
• ECHO (ventricular function, wall motion abN,
valvular dysfunction, Tamponade, PE (spiral
CT and pulmonary angiography)).
• DPL, abdo USS, CT (concealed haemorrhage).
Management
• General measures for all patients with shock.
• Specific appropraiate to aetiology.
Target areas for treatment
• Reduction of metabolic demands
• Adequate O2 provision
• Normalisation of filling
• Manipulation of vasculature with Vasoactive
agents
• Normalization of SV
• Manipulation of pump with Inotropes
CAN WE REDUCE DEMAND?
DO WE EVER DO IT?
Yes!
Yes!
Management - Respiratory
• High flow O2 (improve SaO2 and tissue DO2).
• Ventilatory support or mechanical ventilation
(reduces VO2 by resp muscles).
• Early intubation facilitates invasive
haemodynamic monitoring.
• VO2resp = Oxygen consumed by work of breathing
• VO2tot = Total oxygen consumption
VO2resp as percentage of VO2tot
30
25
20
15
10
5
0
Normals
CTx
surgery
COPD
Pulmonary
oedema
Intensive Care Med. 1995 Mar;21(3):211-7.
So ventilatory support
reduces oxygen demands
In COPD, PS by mask can
reduce this to almost
zero
Ventilatory support
•
•
•
•
•
CPAP:
Recruits alveoli
Improves V/Q
Improves oxygenation
Reduces work of breathing
• BIPAP???
Adequate sedation reduces
oxygen demand
Crit Care Med. 2003 Mar;31(3):830-3.
• 32 post- oesophagectomy/ head and neck malignancies
• All buprenorphine -> Midazolam
– light
– mod
– heavy sedation
OXYGEN CONSUMPTION ml/min/m2
160
140
120
100
80
60
40
20
0
Light
Moderate
Heavy
Paralysis reduces muscle
oxygen consumption
Chest. 1996 Apr;109(4):1038-42.
•
•
•
•
•
•
8 patients
Mean age 63 years
Benzodiazipine + morphine
Then doxacurium paralysis
Mandatory ventilation
O2 consumption measured
OXYGEN CONSUMPTION ml/min/m2
200
180
160
140
120
100
80
60
40
20
0
-paralysis
+paralysis
25% reduction
Cooling reduces
oxygen consumption
Am J Resp Crit Care Med 1995
Jan;151(1):10-4
•12 febrile, critically ill, mechanically ventilated patients
OXYGEN CONSUMPTION ml/min
•T down from 39.4 +/- 0.8 -> 37.0 +/- 0.50C
400
350
300
250
200
150
100
50
0
Hot
Normal
HOW DO WE IMPROVE DELIVERY?
3 ways
• Optimize O2 supplementation to patient
• Optimization of Filling
• Optimization of SV
– Volume
– Vasoactive drugs
– Inotropes
MANAGEMENT OF SHOCK
A: RECOGNISE WHAT TYPE OF SHOCK YOU
ARE DEALING WITH
B: CORRECT THE FILLING STATUS
Empty as a primary cause eg haemorrhage
Empty in sepsis due to increased capacitance
C: ONLY THEN USE VASO-ACTIVE AGENTS:
BETA-1 AGONISTS TO DRIVE THE HEART
ALPHA-1 AGONISTS OR COOLING TO VASOCONSTRICT
GTN OR WARMTH TO VASODILATE
Targets?
HISTORY
• What BP is ‘normal’?
CLINICAL
• Cerebration
• Peripheral perfusion
MONITORING
• Urine (0.5ml/kg/hr minimum)
• ABG (degree of acidosis, trend)
AIM FOR INDICES OF ADEQUATE ORGAN PERFUSION, NOT BP
What is the type of shock?
• Cardiogenic shock – pump failure
– ischaemic / trauma / drugs
• Hypovolaemic shock
– haemorrhage
• Low resistance circulatory / distributive
shock
– drugs / sepsis
Bleed
Diarrhoea
Volume loss
Burns
PE
Tension PTx
Fall in filling
Tamponade
Fall in cardiac
contractility
FALL IN
FLOW
Basic Physiology
PRESSURE = FLOW
X RESISTANCE
BLOOD PRESSURE =
CARDIAC OUTPUT X RESISTANCE
THE RESPONSE IS THE SAME…
Efferent activity to
Medulla falls
Aortic arch and
carotid sinus
baroreceptors
detect a
drop in pressure
Sympathetic efferents
INCREASED SYMPATHETIC ACTIVITY CAUSES
• VENOCONSTRICTION
– INCREASES FILLING PRESSURE AND SUSTAINS
STROKE VOLUME
• POSITIVE INOTROPIC EFFECT
– SUSTAINS STROKE VOLUME
• TACHYCARDIA
– INCREASES CARDIAC OUTPUT
• VASOCONSTRICTION
– INCREASES RESISTANCE
PRESSURE = FLOW (UP) X RESISTANCE (UP)
Management - Fluids
• Optimize preload.
• Restore circulating volume.
• Large vols in HV/septic shock (latter - aim
SvO2 >70% / Hb >10g/dl reduce hosp mort by
16%).
• Judicious vols in CG shock (PAoP/CI).
Filling
200ml COLLOID CHALLENGE
Stroke volume
PAWP
Under filled
Well filled
Over filled
>3mmHg
3mmHg
<3mmHg
Blood volume
Blood volume
20mmHg
LVF: Physiology
Pulmonary
Veins
Pulmonary
Capillaries
LA
MV
At end-diastole, MV is open, flow has ‘ceased’
LV
SO LVEDP = LAP = PVP = PCP
= HYDROSTATIC PCP
Management - Fluids
• CVP surrogate for preload
• Oesophageal doppler better measure of filling
• Fluid should be used to replace that lost
• Aim Hb 7-9 g/dl
• Higher mortality if aim Hb 10-12 g/dl.
Management - Fluids
• Crystalloid vs Colloid…..
• Colloids restore circ vol more efficiently, but no worse
outcome with crystalloid only
• Systematic review colloid use – 4% increase in
mortality (esp HAS)
• SAFE study
• Hypertonic solutions may be useful in pts with cerebral
oedema requiring fluid resuscitation and may reduce
fluid and Blood Tx requirements.
Management - Inotropes
• HV shock – rarely needed – fluids alone
restore CO and BP
• CG shock – fluids not helpful, inotropes
needed
• Septic shock – fluids needed as well as
inotropes
• Both require vasoactive drugs to improve
tissue perfusion and reverse tissue hypoxia.
Inotropic support
RV
SV (ml)
LV
60
5
10
Filling pressure (mmHg)
Management - Inotropes
• CG shock – (low CO/BP and elevated SVR).
• Inodilator (Dobutamine/Milrinone) if BP not
too low.
• Inodilator plus inoconstrictor
(Adrenaline/Dopamine) or vasopressor
(NorAdr) if BP compromised.
• Adr S/E –
hyperglycaemia/hypokalaemia/hyperlactatae
mia (interpret Lactate levels with caution).
Management - Inotropes
• Septic shock – (high CO low BP from
peripheral vasodilatation).
• Firstly optimize preload.
• Then use vasopressor (NorAdr)
• If CO is reduced consider adding
Dobutamine.
• Dopamine (inoconstrictor) could be used but
associated with adverse effects on pituitary
(reduced prolactin/GH/TRH), T-cell function,
gut mucosa perfusion and renal medullary
VO2.
Doses
Dobutamine (5-20µg/kg/min)
–adjust by 2.5µg/kg/min
increments
Adrenaline (start at 0.05µg/kg/min)
–adjust by 0.02µg/kg/min
increment
–GTN to lower resistance
Hypovolaemic shock
• In case of haemorrhagic shock – stop the
bleeding (surgery/radiology/endoscopy)
• Fluid resuscitation
• Correct hypovolaemia/hypoxia/anaemia and
increase DO2 prior to surgery to reduce perioperative mortality
Heart Rate
Blood pressure
CVP
50%
PERCENTAGE BLOOD LOSS
THE SIGNS OF BLEEDING MAY
THEREFORE BE MASKED:
• CVP MAINTAINED
• BLOOD PRESSURE MAINTAINED (NB Postural drop?)
…SO SEEK SIGNS OF
• SYMPATHETIC ACTIVATION
• IMPAIRED PERFUSION
– Clinical
– Acidaemia
Septic shock
• Drain infected fluid collections.
• Antibiotics – broad spectrum – narrowed
cover when culture results available.
• Steroids – 30-120mg/kg methyl pred within 24
hrs onset improve haemodynamic stability
but not survival.
• 100mg hydrocortisone 8 hrly 24-72 hrs after
onset in pts requiring vasopressors with a
sub-N rise in Se cortisol in response to ACTH
(SST) improves haemodynamics and
outcome.
Septic shock
• High volume haemofiltration.
• Used to manage severe metabolic acidosis
and renal failure.
• Cytokines may be removed in the ultrafiltrate
and by adsorption onto the filter and improve
haemodynamic stability.
Cardiogenic shock
• High mortality when complicating acute MI.
• Not reduced significantly by thrombolytic
therapy.
• Angioplasty or CABG should be performed
without delay.
• IABP – useful bridge to surgery in papillary
muscle rupture and ischaemic VSD.
Pathophysiology of cardiac
failure
• Pump failure (ischaemia/drugs/sepsis)
• Ventricular failure
• Reduced SV
– Reduced CO
– Increased baroreceptor activity
• Venoconstriction
• Increased ventricular filling pressure and
myocardial fibre length – increasing
contractility – restoring SV towards normal
LVF: Starling curve
LV and RV curves are splayed
RV
SV (ml)
LV
60
5
10
EDP (mmHg)
Pathophysiology of cardiac
failure
• Eventually the myocardial fibres are unable to
generate further increase in contractility –
resulting in reduction in CO.
• Venous pressure becomes so high that
pulmonary and peripheral oedema ensues.
LVF: Physiology
Alveolus
SURFACE TENSION
RADIUS 4
Starling forces
• The balance of hydrostatic and osmotic
(oncotic) pressures between capillary plasma
and interstitial fluid causes fluid to be filtered
out of the capillary at the alveolar end and
reabsorbed at the venous end
LVF: Physiology
ONCOTIC
PRESSURE
>
Hydrostatic
Pressure
Oncotic
pressure
<
HYDROSTATICP
RESSURE
SURFACE TENSION
RADIUS 4
LVF: Physiology 6
LV FAILURE DEPRESSES THE GRAPH
RV
SV (ml)
LV
60
5
10
Filling pressure (mmHg)
CONSEQUENTLY
In acute depression of LV function:
•
•
•
•
LVEDP rises
LAP rises
PVP rises
PCP rises
Cardiac Failure – vasoactive
drugs
• Optimize / reduce ventricular filling pressure – with
diuretics, venodilators and warmth.
• Reduce cardiac work and increase SV with
vasodilators (eg. GTN or warmth)
• Drive the heart with Beta 1 agonists to increase CO (by
increasing HR)
– CO = HR x SV
• Enhance contractility to increase SV – expense of
increased myocardial work and O2 consumption.
– Aim SV of 1ml/kg
• Cardiac work is determined by CO (vol of blood
pumped) and vascular resistance (resistance against
which it is pumped).
Warning….
• In cardiac failure CO is reduced already.
• Vascular resistance falls further with
vasodilators – which can enhance cardiac
performance.
• Vasodilatation further reduces BP and thus
can impair organ perfusion .
Management - Diuretics
• Use of low-dose “renal-dose” Dopamine to
prevent renal failure in pts with shock does
not reduce the number of pts requiring RRT.
• Natriuesis can be achieved with Frusemide
(bolus 10-80mg or infusion 3-10mg/hr).
• Ensure adequate fluid resuscitation prior to
use.
Frusemide
RV
SV (ml)
LV
60
Diuresis
Filling pressure
(mmHg)
Frusemide
PAWP (mmHg)
Venous Capacitance (ml/100ml)
20
1.2
18
1.1
Venous capacitance
16
1.0
14
PAWP
12
0.9
0.8
n=22
10
0.7
0
20
40
60
80
Time after 0.5-1.0 mg/kg frusemide (mins)
Dikshit et al. N Engl J Med 1973;228:1087-1090.
Nitrates
• Venodilatation
– Reduces LVEDP and PCP
• Vasodilatation
– Increases SV
• CO falls….
Nitrates
PAWP (mmHg)
Cardiac Output (l/min)
3.5
34
Cardiac Output
3.0
32
30
2.5
n=7
2.0
28
1.5
26
24
1.0
PAWP
22
0.5
20
0.0
0
2
4
6
8
Time after 1.6mg sublingual GTN (mins)
10
Bussmann and Schupp Am J Cardiol 1978;41:931-936
Get the filling right
NOW DILATED, YOUR PATIENT MAY
BE UNDERFILLED.
With appropriate monitoring, you may
correct cardiac output with fluid
challenges....
No specific CVP to aim for….
Outcome
• Dependent on: aetiology, severity of illness at
presentation, response to therapy and comorbidities.
• Generally mortality associated with HV shock
is lower than that with CG and septic shock
as long as source of haemorrhage can be
controlled.
• Mortality (even in good centres) septic shock
30-50%, higher in CG shock.
Summary
•
•
•
•
Consider Oxygen Provision in all
Consider Oxygen Consumption in all
Normalise filling
Normalise stroke volume
– Volume
– Dilate
– Inotropes
• Only THEN tinker with raising resistance