Circulatory failure in Intensive Care

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 imbalanceimbalance of delivery relative to need

• This imbalance between supply and demand leads to the development of tissue hypoxiatissue 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

DO2

Oxygen transport

SaO2

Arterial oxygen

saturation

= 1.34

Oxygen content of 1g fully saturated

haemoglobin

x

Arterial Oxygen Content

[Hba]

Arterial haemoglobin concentration

x COx

Cardiac output

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 intra-vascular 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

0

5

10

15

20

25

30

Normals CTxsurgery

COPD PulmonaryoedemaV

O2r

esp

as

per

cen

tag

e o

f V

O2t

ot

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

0

20

40

60

80

100

120

140

160

Light Moderate HeavyOX

YG

EN

CO

NS

UM

PT

ION

ml/m

in/m

2

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

0

20

40

60

80

100

120

140

160

180

200

-paralysis +paralysisOX

YG

EN

CO

NS

UM

PT

ION

ml/m

in/m

2

25% reduction

Cooling reduces

oxygen consumption

Am J Resp Crit Care Med 1995 Jan;151(1):10-4

0

50

100

150

200

250

300

350

400

Hot Normal

OX

YG

EN

CO

NS

UM

PT

ION

ml/m

in

•12 febrile, critically ill, mechanically ventilated patients

•T down from 39.4 +/- 0.8 -> 37.0 +/- 0.50C

HOW DO WE IMPROVE DELIVERY?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 THENC: 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?

HISTORYHISTORY• What BP is ‘normal’?

CLINICALCLINICAL• Cerebration• Peripheral perfusion

MONITORINGMONITORING• Urine (0.5ml/kg/hr minimum)• ABG (degree of acidosis, trend)

AIM FOR INDICES OF ADEQUATE ORGAN PERFUSION, NOT BPAIM 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

FALL IN FLOW

Volume loss

Bleed

Diarrhoea

Burns

Fall in filling

PE

Tension PTx

Tamponade

Fall in cardiac contractility

Basic Physiology

= FLOW

BLOOD PRESSURE = CARDIAC OUTPUT X RESISTANCE

PRESSURE X RESISTANCE

Aortic arch and carotid sinus baroreceptors detect a drop in pressure

Efferent activity to Medulla falls

Sympathetic efferents

THE RESPONSE IS THE SAME…

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).

200ml COLLOID CHALLENGEUnder filled

<3mmHg

Well filled

3mmHg

Over filled

>3mmHg

Stroke volume PAWP

Blood volume Blood volume

20mmHg

Filling

LVF: Physiology

Pulmonary Capillaries

Pulmonary Veins

LA

LV

MVAt end-diastole, MV is open, flow has ‘ceased’

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

Filling pressure (mmHg)

SV (ml)

5

60

RV

LV

10

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/hyperlactataemia (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 peri-operative mortality

Heart Rate

Blood pressure

CVP

50%PERCENTAGE BLOOD LOSS

THE SIGNS OF BLEEDING MAY THE SIGNS OF BLEEDING MAY

THEREFORE BE MASKED:THEREFORE BE MASKED:• CVP MAINTAINED

• BLOOD PRESSURE MAINTAINED (NB Postural drop?)

……SO SEEK SIGNS OF SO SEEK SIGNS OF • SYMPATHETIC ACTIVATION SYMPATHETIC ACTIVATION

• IMPAIRED PERFUSION 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

LV and RV curves are splayed

EDP (mmHg)

SV (ml)

5

60

RV

LV

10

LVF: Starling curve

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

SURFACE TENSION RADIUS 4

Alveolus

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

HYDROSTATICPRESSURE<

SURFACE TENSION RADIUS 4

LV FAILURE DEPRESSES THE GRAPH

Filling pressure (mmHg)

SV (ml)

5

60

RV

LV

10

LVF: Physiology 6

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

SV (ml)

Filling pressure (mmHg)

60

RV

LV

Diuresis

Dikshit et al. N Engl J Med 1973;228:1087-1090.

0 20 40 60 80

10

12

14

16

18

20

Time after 0.5-1.0 mg/kg frusemide (mins)

PAWP

n=22

PAWP (mmHg)

0.7

0.8

0.9

1.0

1.1

1.2

Venous capacitance

Venous Capacitance (ml/100ml)

Frusemide

Nitrates

• Venodilatation– Reduces LVEDP and PCP

• Vasodilatation– Increases SV

• CO falls….

Bussmann and Schupp Am J Cardiol 1978;41:931-936

0 2 4 6 8 10

20

22

24

26

28

30

32

34

Time after 1.6mg sublingual GTN (mins)

n=7

PAWP

PAWP (mmHg)

0.0

0.5

1.0

1.5

2.0

2.5

3.0

3.5

Cardiac Output

Cardiac Output (l/min)

Nitrates

NOW DILATED, YOUR PATIENT MAY BE UNDERFILLED.

With appropriate monitoring, you may correct cardiac output with fluid challenges....

No specific CVP to aim for….

Get the filling right

Outcome

• Dependent on: aetiology, severity of illness at presentation, response to therapy and co-morbidities.

• 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