AIRWAY, BREATHING

& CIRCULATION
IN EWS
Dr. Rumaisah Satyawati Sp.An, KIC

OBJECTIVE
Recognise
when difficulties with a patients airway or breathing may
compromise oxygen delivery to the tissues
Apply
the appropriate oxygen delivery device
Manage
ppropriately a patient with impaired arterial oxygenation
Explain
why the respiratory rate is such an important marker of
the deteriorating patient.

AIRWAY

INTRODUCTION

For oxygen to reach haemoglobin and be transported around

the body to the tissues, it needs to pass through the upper and
lower airways of the lungs to the alveoli.

Need both a patent airway, and an intact respiratory nerve an

muscle function to move air in and out of the lungs.

Oxygen in the alveoli will diffuses across the thin alveolar capilla
membrane into the blood, and attaches to haemoglobin.

It is dependent on the pulmonary & then the systemic blood

circulation to move the oxygen to the tissues and cells.

Adult Airway
Oxygen cannot move into the lower
respiratory tract unless the airway is patent.
Causes of airway obstruction can either be
mechanical or functional.

Causes of airway
obstruction
Functional airway obstruction
unconsciousness,the muscles relax
and allow the tongue to fall back
Mechanical airway obstruction
Aspiration of a foreign body
Swelling/bleeding in the upper
airway (e.g. trauma, allergy and
infection).
Oedema or spasm of the larynx.

Examination of the Airwa

Management of the Obstructed

Airway

In the majority of patients in hospital, the patients

airway obstruction is functional, i.e. due to a
depressed level of consciousness.
1.Head tilt
2.Chin lift
3.Jaw thrust
4.Insertion of an oropharyngeal or nasopharyngeal
airway.

Management of the Obstructed Airw

chin-lift

Management of the Obstructed Airw

Head Tilt

Management of the Obstructed Airw

Management of the Obstructed Airw

Continues
a depressed level of
consciousness/ unable to protect
airway :
Endotracheal intubation
by experienced staff.
Surgical airway
by competent,
experienced staff.

Airway obstruction

Cannot maintain airway

( Mechanical factor : airway
sweeling , post op haematoma
infection )

Activate the cardiac arrest

system
(inculding anesthesia )

Breathing

Breathing

Breathing is required to move adequate oxygen into

and carbon dioxide out of the lungs.

Breathing requires:
1. Intact respiratory centre in the brain
2. Intact nervous pathways from brain to diaphragm
and intercostals muscles
3. Adequate diaphragmatic & intercostals muscle
function
4. Unobstructed air flow (large and small airways)

Breathing : Problem Reconition

Look
Listen
Feel

Assess
Look

Respiratory rate important marker

1st thing you notice.

Look for signs :

Abnormal respiratory rate
Use of accessory respiratory muscl
Sweating/pallor
Central cyanosis
Abdominal breathing
Shallow breathing
Unequal chest movement

Breathing : Problem Reconition

Assess
Listen

Look

Noisy secretions in the upper airwa

Stridor or wheeze partial obstructio

Listen
Feel

Auscultate :
Quiet or absent breath a
pneumothorax or a pleural effusion

Bronchial breathing consolidation

Breathing : Problem Reconition

Assess
Feel

Look
Listen
Feel

Palpation tracheal & chest wall

Tracheal deviation mediastinal shift :
Pneumothorax
pleural fluid-tracheal deviation away
from the lesion
Lung collapse-tracheal deviation toward
the lesion
Percussion:
Hyper-resonance pneumothorax
Dullness consolidation or pleural fluid

Why Respiratory Rate is Important ?

RR >>
Reflect a drop in arterial blood O2 saturation level

An important indicator of inadequate DO2 to the tissu

A marker of a deteriorating patient.

Respiratory rate, SpO2 EWS

Adult Respiratory EWS

Normal Arterial Saturation and

Tachypnoea
Decreased DO2
-RR increased : can occur in patients with normal
or low SaO2
-RR increased : better indicator of a
deteriorating patient than arterial oxygen
saturation.

Management
All deteriorating patients should
receive
oxygen
Supplemental O2 to achieve :
SpO2 of 96%,
PaO2 as close to 13kPa as possible, but at
least 8kPa (SaO2 90%) is essential.
Sitting them upright , O2 12-15 litres/min
NRM
Does not improve require review by an
anaesthetist

 COPD

CO2 retainers
Risk factors for
hypercapnoeic resp failure
(morbid obesity, chest wall
deformities / neuromuscular
disorders

High O2
Suppressing
hypoxic drive

Blood oxygen levels fall too low

end-organ damage/ cardiac arres
The aim of care PaO2 8kPa or SpO2 > 90%
COPD PCO2

> 8kPa, PO2< 8kPa do not turn the inhaled O2

PO2 > 8kPa turn the inhaled O2 down to maintain SaO2 90%

Oxygen Delivery Systems

Fixed performance devices
Variable performance devices

Oxygen Delivery Systems

Fixed Performance Devices
The inspired O2 concentration depend on:
A. Oxygen flow rate
B. Attached diluter (the Venturi mask )
Risk of hypercapnia Venturi system
is more accurate in delivering the O2
concentration desired.

Oxygen Delivery Systems

Variable performance devices
The inspired O2 concentration will depend o
A) Oxygen flow rate
B) The patients ventilatory pattern

Variable performance devices

Nasal prongs
The dead space of the
nasopharynx reservoir
When the patient inspires,
entrained air mixes with reservoir
air enriching the inspired gas.
Oxygen flow rates of 2-4L/min

High flow nasal prongs

These use warm humidified oxygen
at higher flow rates 4-8L/min

Variable performance devices

Oxygen facemasks
Reservoir volume of oxygen is
increased above that achieved by
the nasopharynx
Higher oxygen concentration can be
achieved in inspired gas (max 5060%)

Non-re-breathermask
A simple face mask with the
addition of a reservoir bag,
With 1 or 2 valves over the
exhalation ports prevent exhaled
gas entering the reservoir bag.
Permits inspired oxygen
concentration up to

90%.
O2 flow rate of 12-15L/min.

Monitoring and Titrating Oxygen Therapy

Clinically
patients colour,
Respiratory rate,
Respiratory distress
Measuring arterial oxygenation
Pulse oximetry
Arterial blood gas (O2 & CO2 are measured, the
metabolic status , including lactate).

Monitoring and Titrating Oxygen Ther

CO2 tension rises + acute respiratory failure,
tiring ventilatory support

If CO2 begins to rise in COPD reduce the inspired

O2 concentration arterial oxygen tension should
not be allowed to fall < a PO2 of 8 kPa.

Patients do not die from a raised CO2 alone: they die

from hypoxaemia

Monitoring and Titrating Oxygen The

As long as the concentration of oxygen being

delivered is recorded,
the degree of hypoxaemia can be calculated

The blood gas machine can calculate as long as th

correct inspired oxygen concentration is recorded.

Directly

Indirectly

SaO2
SpO2
The ratio of O2 carying
Pulse oximetry
haemoglobin compared to oxyhaemoglobin concentration a
the total amount of a percentage of total haemoglobi
haemoglobin

Oximeters can be unreliable :

- Poor Peripheral circulation
- cold environment
- Arrhythmias,
- Convulsing or shivering,

BUT carbon dioxide levels are not measured

ABGs remain the gold

standard assessing
respiratory failure.
it measures
Arterial oxygen,
Arterial saturation and
Arterial carbon dioxide.
Metabolic system
(bicarbonate concentration,
base excess & lactate)
an approximate Hb
electrolytes
blood glucose.

ABGs should be
measured in :
Critically ill
Deteriorating O2
saturations
Increasing RR

ABGs should be measured in

Critically ill

Have deteriorating
oxygen saturations or
increasing RR
Requires significantly increased supplemental
oxygen to maintain O2 saturation

Have risk respiratory

factors for hypercapnoeic
failure
Have poor peripheral circulation &

therefore
unreliable peripheral measurements of O2
saturation.

If you suspect failing oxygen delivery, consider where in the oxy

delivery chain may be disordered.

ABC - Oxygen Delivery Chain

Summary
Increase in RR can occur even though SaO2 may be
normal
Airway obstruction may be due to mechanical factors
not be so easily treated medical emergency
requires activation of the cardiac arrest system
(including anaesthesia) or ERS

COPD & CO2 retainers : high conc inspired O2 suppressing

their hypoxic drive.
Blood O2 levels fall too low end-organ damage or cardiac
arrest
The aim PaO2 of 8kPa, SpO2 > 90%

COPD with PCO2 >8kPa & hypoxic, PO2<8kPa do NOT turn the
inhaled O2 down & do not leave them unattended.
PO2 is>8kPa can turn inhaled O2 down to maintain
SaO2>90%.

Acutely ill pts unnecessary to remove the O2 mask when tak

ABGs, as it may precipitate sudden deterioration.

If the pulse oximeter does not provide a reading, do not assume

is broken, the patient may have poor perfusion and be very
unwell!!

O2 saturation may be normal but the PCO2 may be high

reflecting inadequate minute ventilation and respiratory failure
Incorporate all the vital signs in your assessment.
Respiratory score of 3 requires immediate review by doctor

Circulation

The Importance of Oxygen

Oxygen deliverys key components are:

Cardiac output = Stroke Volume x Heart Rate

Arterial oxygen content =
Haemoglobin concentration x Arterial Oxygen Saturati

The Importance of Oxygen

Oxygen reaching the cells and mitochondria is

dependent upon adequate amounts of oxygen bein
delivered via the blood circulation
Without oxygen being delivered to the
mitochondria, inadequate amounts of ATP are
generated and cellular dysfunction occurs.

Blood Pressure, Heart Rate and Oxygen

Delivery
Blood pressure is the product of cardiac output and
total peripheral resistance (TPR)

BP low reflect CO low lead reduction Do2

High HR reflect low SV low reflect low CO

lead inadequate O2 to the tissues.

Hence HR & BP : important surrogate markers
adequate CO & DO2

Calculation of Adult EWS for heart rate:

Blood Pressure and Maintenance of Organ

Function
some organs that require an adequate blood
pressure The brain & kidney
Calculation of Adult EWS for blood pressure:

A systolic BP greater than or equal to 200 requires a

doctor to review

Definition of Hypotension

The generally acceptable definition of hypotension

in adults is:
A drop of more than 20% from usual blood
pressure or
Systolic blood pressure of less than 100mmHg

Possible Causes of Hypotension

Blood pressure can either fall because of:

1. A fall in cardiac output
2. A fall in peripheral vascular resistance

Cardiac output : Stroke Volume x Heart Rat

Cardiac contractility

Pre-loa

load

Venous return
Major negative influences
Resistance
(negative inotropy) i: : Intravascular blood volume
of the
Myocardial ischaemia
ejection of
Absolute:
cidosis
Drugs ( B-blockers, anti- Decrease : bleeding,
blood from
electrolyte, water loss,
dysrhythmic)
the ventricle
diarrhoea, vomiting,
- aortic
Major positive influences diabetes insipidus
stenosis.
Relative:
(inotropy) i:
Sympathetic nervous Vasodilatation & pooling
(vasodilators, epidurals,
system
sepsis)
Sympathomimetics
(noradrenaline, adrenaline)
Intrathoracic pressure
Calcium
increase : asthmatic attack,
Digoxin
PPV

B. Heart rate

* Faster HR can increase CO = occurs when Falling S

* Reduction HR can decrease CO

* Does a fast heart rate always increase cardiac out

and blood pressure?

Faster HR may reduce CO.

If the ventricle does not have adequate time to fill with
blood reduces SV .
As a result CO may cause a drop BP ( atrial fibrillatio
with a rapid ventricular response)

* Does a slow heart rate always decrease

cardiac output and blood pressure?
Slow HR may be no reduction CO & BP
- ventricle has a longer time to fill
- the end diastolic volume is increased
- increases the stroke volume per beat.
- very healthy athlete.

C. Peripheral Vascular Resistance

Changes PVR increase or decrease BP
Increase PVR Autonomic Nervous System
a. Stimulation of Sympathetic Rec
vasoconstriction & increase BP (noradrenaline,
adrenaline )
b. Direct action on arteriole smooth muscle (
vasopressin, angiotensin, methylene blue )
vasoconstrictor by inhibiting nitric oxide

Decrease in peripheral vascular resistance

Blockage of Autonomic Sympathetic Nervous System

Increasing the stimulation of the baroreceptors. Drug that blo
the sympathetic nervous system c
vasodilatation(clonidine,epidurals)

a.

b.

Direct action on arteriole smooth muscle molecules an

drugs can have a direct effect on the vascular smooth muscl
arterioles, causing vasodilatation.
Vasodilating drugs
Calcium channel blockers, ACE inhibitors
Vasodilating Molecules
Nitric Oxide (infection/sepsis)
Vasodilating conditions
Acidosis, increase in temperature

Compensatory Mechanisms for Hypotensi

A. Reduction in Cardiac Output

Compensatory Mechanisms for Hypotensio

2.Reduction in Heart Rate

Compensatory Mechanisms for

Hypotension
B. Reduction in Peripheral Vascular Resistanc

Consequences of Hypotensio

The Initial Management of Hypotension

Management Plan
Fall in peripheral vascular resistance
Tachycardia, organ failure, lactate formation (-)
close monitoring vs EWS escalation protocol

1.

2. Tachycardia (+), organ failure & lactate formation (-)

low

venous return & SV

-

Intravenous fluid bolus (500-1000 mls)

Improvement compensation NOTE

not resolved repeat the fluid challenge

Consider Sepsis Six regimen

- Continues hypotension, tachycardia a,warm hands, furthe

fluid + doctors if there are no signs of heart failure.

-intensive care review should be requested when 3 litres of flu

The Initial Management of Hypotension

Management Plan
Fall in peripheral vascular resistance
Hypotension
and evidence of organ failure
3.
Intravenous
fluid bolus (500-1000 mls)
not
- resolved repeat the fluid challenge
Continues
hypotension, tachycardia a,warm hands
further fluid + doctors if there are no signs o
heart failure.
- intensive care review should be requested when
litres of fluid
- Call for an intensive care review particularly if th
patient has received three litres of fluid or signs o
organ failure persist.

The Initial Management of Hypotension

1.

Management Plan
Fall in Cardiac Output
Fall in Pre-Load

History , Examination , Laboratory Investigations

Correct cause of loss of fluid
Replace whatever fluid
Estimate how much has been lost
blood
pump set through a large bore intravenous cannula
Continue
fluid rapidly until there is the desired response: B
HR returning to normal
Improvement in organ function, (urine output )
ntensive
care should be alerted especially if there are no s
of improvement despite administering 3L of fluid.
-

The Initial Management of Hypotension

Management Plan
Fall in Cardiac Output
2.Fall

in contractility

myocardial ischaemia or infarction

History , Examination , Laboratory Investigations
Clinical Management :
cardiogenic shock inotropic support & referral to
ICU

Stop all intravenous fluids as the patient is by

definition fluid overloaded, Continue strict
monitoring of fluid balance

Myocardial infarction protocol if MI confirmed

Summary

Blood pressure = Cardiac Output x Peripheral Vascular Resista

Hypotension:
High HR & low BP may reflect low DO2
Pts normally hypertensive may be relatively hypotensive ev
when their systolic blood pressure is above 100mmHg
In adults do not always use 100mmHg as your CRITICAL
Systolic Blood Pressure cut off!
Hypotension can be a marker of a deteriorating patient wh
at risk of increased risk of death.
A shocked patient has signs of organ failure which may or
not accompany hypotension.
Decrease in CO can be caused by:
Decreases in intravascular blood volume
Increases in ITP, Increase in peripheral vascular resistanc

Any decrease in CO can cause a decrease in DO2 !

The greatest concern is that hypotension may suggest that the
an inadequate amount of O2 getting to the tissues, which is
described as SHOCK.

General Management Guidelines for hypotension in adults:

Hypotension and warm hands : Administer fluids
Hypotension, cool hands, no signs of heart failure : Administer fl
Hypotension, cool hands, signs of heart failure : Cease fluids. Re
CCU/ICU for inotropes.

Remember to incorporate all the vital signs in your assessmen

A SYSTOLIC BLOOD PRESSURE 90mmHg in adults

requires immediate review by a doctor, consider activa
of the ERS.

THANK YOU