Compass Training Manual

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Pointing you in the right direction

DR.BRONWYN AVARD

NICOLE SLATER

HEATHER MCKAY

DR. KATHYRN DAVESON

DR. PAUL LAMBERTH

DR.IMOGEN MITCHELL


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COMPASS 2006

The design, layout, and publication of the CD by ACT Publishing.

For enquires about the COMPASS course or copies of the manual contact:Heather Mckay

Project OfficerACT [email protected] 6244 3885

Disclaimer

The authors or ACT Health cannot be held responsible for any loss,damage, or injury incurred by any individual or groups using this manual.

First edition November 2006

All rights reserved: no part of this publication may be photocopied,recorded or otherwise reproduced, stored in a retrieval system ortransmitted in any form by any electrical or mechanical means, without

the prior permission of:

Patient Safety & Quality UnitACT Health


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CONTENTS

Introduction Page 4

Modified Early Warning Scores Page 8

Oxygen Delivery Page 16

Airway & Breathing Page 21

Circulation Page 36

Urine Output & Central Nervous System Page 59

Communication, Team Work & Management Plans Page 77

References Page 93


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Introduction

COMPASS is an interdisciplinary education program designed to enhance

our understanding of patients deteriorating and the significance ofaltered observations. It also seeks to improve communication betweenhealth care professionals and enhance timely management of patients.This education package has been developed in conjunction with thedevelopment and implementation of a Modified Early Warning Score anda redesigned general observation chart.

Preamble

It has become increasingly apparent that many doctors and nursingstaff are unable to manage a deteriorating patient in an appropriate,timely fashion. This is often as a result of the inability of recognisingthat the patient is deteriorating. Delaying resuscitation and treatmentincreases the likelihood of organs failing due to inadequate oxygendelivery to these tissues. This in turn can lead to unexpected death,

unexpected cardiac arrests and unplanned admissions to the intensivecare unit.

It is important to understand the key components that lead toappropriate management.

A.Absence of observationsa. Equipment not availableb. Equipment malfunctioningc. Inability to use equipment due to lack of knowledged. Inadequate time to perform observationse. Inability to make time for performing observationsf. Lack of understanding of why observations are importantg. General culture that observations are not important


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B.Inability to understand observations recordeda. Unable to trend results and interpret the meaning

b.

Lack of knowledge

C.Failure to trigger timely appropriate responsea. Absence of observations to make an interpretationb. Inability to understand observations recordedc. Inability to develop a diagnosisd. Inability to develop a treatment plan

Having identified the key components, it is possible to address areasthat pertain to lack of knowledge.

An example of what can go wrong:

60 yr old male who wanted active treatment and this was expressed anddocumented.

The patient met the Medical Emergency Team (MET) criteriabut the MET was not called. Over a period of twenty-four hoursthere were thirteen occurrences of hypotension, with thesystolic blood pressure ranging from 64 to 86 mmHg during thistime.

Respiratory Rate was inconsistently documented. Despite the BP being unresponsive to treatment administered,

there was no escalation of either treatment or degree ofcommunication by ward staff.

The patient was being treated by an Resident Medical Officerwithout being reviewed by a more senior doctor.

Patient first met the MET criteria at 2130 but was never called. Seen by a registrar 15 hours later.

The patient died the following day.It is episodes like this that we want to prevent.


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Our Aim

To enable health care professionals to recognise the deterioratingpatient and initiate appropriate and timely interventions

Our Objectives

For participants to understand the importance and relevanceof observations and the underlying physiology.

For participants to be able to recognise and interpret

abnormal observations For participants to be able to communicate effectively to the

right people and at the right time. For participants to feel confident in recognising and

managing deteriorating patients To facilitate teamwork within the multidisciplinary team To enable nurses, doctors, and physiotherapists to develop

management plans together

How it works

There are three phases to the package to be completed in the followingorder:

The CD to be worked through independently An online quiz

A 3 hour face-to-face session

On the CD enclosed you will be guided through a case study. You will have access to their history, the current situation, and

their observation charts and fluid balance. A series of questions will be asked which will then direct you to

information on the specific vital sign in question.


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In order to move on to the next section on a different vital signyou must correctly answer a multiple-choice question.

If you get any wrong you will be directed back to the

information just covered to reinforce the information in thatsection. When you answer the questions correctly you will move on to the

next section of the case study.

Once you have completed the case study you will proceed to a multiple-choice quiz to test your knowledge. You will be unable to skip ahead inthe CD, however you will be able to go back to any area that you have

already completed if you choose to. The CD MUSTbe completed prior tocoming to the face-to-face session you have been scheduled for. Youmust also go to an internet terminal and access an online quiz. This againis multiple choice and MUST be completed prior to the final session.Your results will be available to the program coordinator.

OK LETS GET STARTED!!!!!!!!


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Modified Early

Warning Scores


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Modified Early Warning Scores

Learning Objectives: Be able to calculate a Modified Early Warning Score Be aware of your responsibilities when a trigger score (see

text box 1) is met Understand how to complete the new observation chart

A vital sign is a sign that pertains to life without which life wouldnot exist. Derangements in pulse and blood pressure measurements

can reflect an increased risk of life not existing and so can beconsidered a vital sign.

If derangements in pulse and blood pressure measurements reflectan increase in the risk of death, it is important that these signs aredetected early and appropriate treatment is delivered to not onlynormalise these signs but also decrease the risk of the patientdying.

A Modified Early Warning Score3 (MEWS) is a simple bedside scorethat is calculated by nursing staff from the observations taken, toindicate early signs of a patients deterioration. It is a valuable tool,in particular in acute wards where patients are often quite unwelland there may be many inexperienced staff. Vital signs only includeHeart Rate, Blood Pressure, Temperature, and Respiratory rate,however MEWS takes into account of other observations as well.

The MEWS looks at all the observations together, not just a singleobservation in isolation. It includes respiratory rate, oxygensaturations, temperature, blood pressure, heart rate, sedationscore, and urine output.


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Trigger Score:A score of 4 is the initial trigger point for action, with escalated

notification at 6 and 8.

Text box 1: Trigger Score

It includes: A flow chart to direct nurses who needs to be notified and

at what point. A structure for increasing the frequency of observation

once a trigger score is reached. A guide as to what escort is required if the patient is to be

transferred to another clinical area, e.g. medical imaging

It is beneficial as it: provides a structure for communicating the changes in vital

signs and observations and empowers nurses to take action.It does not replace MET (see text box 2).

assists doctors in prioritising the management of theirpatients.

prompts more timely review and treatment of patients as ithas an inbuilt escalation policy if the patient has not beenreviewed in the required time frame.


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Text box 2: MET

To obtain the MEWS each individual observation (table 1) is scoredaccording to the criteria in table below.

Table 1: MEWS

MEWS does NOT replace calling the Medical Emergency

Team (MET). If the patient meets the MET criteria a

Code Blue/MET should be called as per MET protocol.

MET Criteria:

All respiratory & cardiac arrests

Threatened Airway, RR < 5 or > 36

Pulse < 40 or > 140

Systolic BP < 90

Sudden fall in level of consciousness, fall of GCS > 2, repeated orprolonged seizures

Any patient you are seriously worried about that does not fit theabove criteria.

MEWS Score 3 2 1 0 1 2 3

Resp Rate < 8 9-20 21-30 31-35 > 36

SpO2 < 84 85-89 90-92 > 93

Temperature < 34 34.1-35 35.1-36 36.1-37.9 38-38.5 > 38.6

Heart Rate < 40 40-50 51-99 100-110 111-130 >130Blood pressure See chart

Sedation score 0-1 2 3 4

Urine for 4 hrs 800


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To obtain the blood pressure score the patients usual systolic bloodpressure MUSTbe determined in consultation with the medical staffand written in the box provided.

The current systolic blood pressure reading is then compared in thetable below to establish the blood pressure score4.

Table 2: Blood pressure score

The MEWS is calculated and documented on the new Observation Chart.If a different chart is being used the MEWS score is still required tobe calculated and recorded.

Additional considerations relating to the MEWS for the individualpatient can be documented in the space provided at the top of the bloodpressure table (i.e. chronic lung disease, dialysis patients).

Patients Usual Systolic Blood Pressure

Additional Considerations

Usual SBP 190 180 170 160 150 140 130 120 110 100 90 80

200s 0 0 1 1 2 2 2 3 3 4 5 5190s 0 0 0 1 1 1 2 2 3 3 4 4180s 0 0 0 0 0 1 1 2 2 3 3 4

170s 1 0 0 0 0 1 1 2 2 3 3 3160s 1 1 0 0 0 0 0 1 1 2 2 2

150s 1 1 1 0 0 0 0 0 1 1 2 2

140s 2 1 1 1 0 0 0 0 0 1 1 1

130s 2 2 1 1 0 0 0 0 0 0 0 1

120s 2 2 2 1 1 0 0 0 0 0 0 0110s 3 2 2 2 1 1 0 0 0 0 0 0100s 3 3 3 2 2 2 1 1 0 0 0 090s 4 3 3 3 2 2 2 2 1 1 0 080s MET 2 1 0

Curre

nt

Blood

Pressure

70sMET 4 MET 3

MET 1


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MEWS > 4

Increase the frequency of observations

Notify medical staff Patient requires an escort

Text box 3: Activation protocol

If the total MEWS reaches an initial trigger point of 4 theactivation protocol (text box 3) is to be initiated.

A. Increase Frequency of ObservationsIf the score is equal to or greater than 4, the frequency ofobservations is escalated to2: hourly for the first hour (or more frequently if the

patients condition dictates). Then hourly for the next four hours if MEWS is


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MEWS > 4 MEWS > 6 MEW S > 8

Registrar & VM O n otified, Registrar to review within 10 minutes. Noresponse from the page or the treatment, the MEW S has not

decreased consider MET/ICU consult

Contact RMO, to

review within 30minutes.

Contact Registrar & RMO , to review in 30minutes

After 60 mins ptnot reviewed &MEWS has not

decreased

After 60 mins ptnot reviewed &MEWS has not

decreased

Figure 1: Notification flowchart

C. Type of Escort Required Out of WardIf the trigger score is reached, the following guide for whoshould accompany the patient is to be used if the patientrequires escort out of the ward area2.

MEWS > 4 Registered Nurse MEWS > 6 Registered Nurse & Intern MEWS > 8 Registered Nurse & Registrar

At the time of reaching a trigger score the nurse MUST

always notify the team leader or CNC.

Text box 4: CNC notification


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Summary

Trigger Score: A score of 4 is the initial trigger point for action,

with escalated notification at 6 and 8. MEWS does NOT replace calling the Medical Emergency Team

(MET). If the patient meets the MET criteria a code blue/METshould be called.

MET Criteria:o All respiratory & cardiac arrestso Threatened airway, RR < 5 or > 36o Pulse < 40 or > 140o Systolic BP < 90o Sudden fall in consciousness, fall of GCS > 2, repeated or

prolonged seizureso Any patient that you are seriously worried about that does not

fit the above criteria. MEWS > 4

o Increase the frequency of observations

o

Notify medical staffo Patient requires an escort

At the time of reaching a trigger score the nurse MUST

always notify the team leader or CNC.

In the next few sections you will be taken through each observation

individually. Always remember though that you must look at all the

observations as a whole when assessing the patient, and not just asingle parameter in isolation. The aim is for you to understand allthe changes that are occurring and what might be causing them.


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Oxygen Delivery


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Oxygen Delivery

Learning Objectives:

To understand the importance of oxygen delivery at the tissue level To understand the factors that affect adequate oxygen delivery

Adenosine triphosphate (ATP) is required as a source of energy for all

intracellular functions.ATP is formed in the mitochondria via phosphorylation. A phosphate isadded to adenosine diphosphate (ADP) via a high-energy bond, thusforming ATP. This stores energy on a temporary basis. When energy isneeded by the cell, ATP is dephosphorylated to ADP, releasing theenergy from the bond (see text box 5).

ATP ADP + Pi + Energy(Adenosine + Pi + Pi + Pi) (Adenosine + Pi + Pi )

Text box 5: Energy release

Oxygen is essential for the adequate production of ATP by cell

mitochondria (see figure 2). If there is inadequate oxygen supply, ATPproduction falls, and cellular function is then depressed (see figure 3).


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1Glucose

Glucose-6-Phosphate

CYTOPLASM

2Pyruvate

pyruvate dehydrogenase

3Pyruvate Acetyl CoA + 2ATP

4Citrate, TCA cycle/Krebs

NADH NAD ++

H+ + O2 H20

ADP + Pi3P 36ATP

FIGURE 2: AEROBIC METABOLISM (i.e. with oxygen)

MITOCHONDRIA


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1Glucose

Glucose-6-Phosphate

CYTOPLASM

2Pyruvate




Figure 3: ANAEROBIC METABOLISM (i.e. in the absence of oxygen)

Oxygen supply to the cells can be described by the oxygen deliverychain (see figure 4).

MITOCHONDRIA

LACTATE


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Oxygen Delivery = Cardiac Output x Arterial Oxygen content

Thus oxygen delivery requiresA. Arterial oxygen content:

a) haemoglobin concentration ([Hb)]b) haemoglobin oxygen saturation (SaO2)c) partial pressure of oxygen (PaO2)

SEE SECTION ON AIRWAY AND BREATHING

B. Cardiac output SEE SECTION ON CIRCULATION

FIGURE 4: ABC and the Oxygen Delivery Chain


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Airway and Breathing


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Airway and Breathing

Learning Objectives:

To recognise when difficulties with airway or breathing arecompromising oxygen delivery to the tissues

To be able to apply the appropriate oxygen delivery device To be able to appropriately manage a patient with impaired arterial

oxygenation

INTRODUCTION

In order for oxygen to reach haemoglobin, and be transported aroundthe body to the tissues, it needs to pass through the upper airways(nose, mouth,trachea) and lower airways of the lungs (bronchi) to thealveoli. To do this, we need both a patent airway, and the respiratorynerve and muscle function to move air in and out of the lungs. Onceoxygen is in the alveoli, it diffuses across the thin alveocapillary

membrane, into the blood and attaches to haemoglobin. From here, it isdependent on pulmonary and then systemic blood flow to move oxygen tothe tissues and cells where it is required.

AIRWAY

Oxygen cannot move into the lower respiratory tract unless the airwayis patent.Airway obstruction can either be mechanical or functional.

A. Functional airway obstruction - May result from decreased levelof consciousness. This is most commonly due to obstruction ofthe pharynx by the tongue, which can fall backwards whennormal muscle tone is reduced.


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B.Mechanical airway obstruction - May be through aspiration of aforeign body or swelling/bleeding in the upper airway (e.g. trauma,allergy, and infection). It may also be caused by oedema or spasm

of the larynx.

Examination

Airway patency should always be assessed firstABC. Recognition ofairway obstruction is possible using a look, listen, feel approach.

Look: complete airway obstruction can cause paradoxical chest andabdominal movements (see-saw like movement, where inspirationis associated with outward movement of the chest, but inwardmovement of the abdomen)Other signs of airway obstruction include use of accessorymuscles (neck and shoulder muscles), and tracheal tug

Listen: in complete airway obstruction, there will be no breathsounds at the mouth or nose; in incomplete obstruction, breathingwill be noisy and breath sounds are reduced (stridor= inspiratorywheeze)

Feel: placing your hand immediately in front of the patients mouthallows you to feel if there is any air moving

Management

In the majority of cases in hospital, airway obstruction is functional, i.e.due to depressed level of consciousness. Simple manoeuvres may berequired to open the airway :

A.

chin lift (see figure 5)B. jaw thrustC. head tiltD. insertion of an oropharyngeal or nasopharyngeal airway

(Guedels airway)


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FIGURE 5: Simple Airway Manoeuvres

Image courtesy of Mayo Healthcare Pty Ltd

Suctioning may be required to remove any vomitus or secretions, whichcould be contributing to airway obstruction.If the patient continues to have a depressed level of consciousness andis unable to maintain their airway (see text box 6), intubation may berequired, which needs to be performed by experienced staff.

In rare cases, the airway obstruction may be due to mechanicalfactors, which are not so easily treated, e.g. airway swelling,post-operative haematoma, infection. This is a medicalemergency. A Code Blue/MET should be called.

Text box 6: Airway obstruction

A surgical airway may be required if intubation is not possible (called acricothyroidotomy), and this should only be attempted by experiencedstaff.


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BREATHING

Breathing is required to move adequate oxygen in and carbon dioxide outof the lungs. Breathing requiresa) intact respiratory centre in the brainb) intact nervous pathways from brain to diaphragm &

intercostal musclesc) adequate diaphragmatic & intercostal functiond) unobstructed air flow (large and small airways)

Respiratory rate is an early indicator of falling oxygen delivery. Asoxygen delivery to the tissues is reduced, cells revert to anaerobicmetabolism. This increases lactate production, resulting in build up ofacid (see figure 6). The accumulation of lactic acid stimulates anincrease in respiratory rate (tachypnoea).

Decreased oxygen delivery at the tissue level

Anaerobic metabolism

Lactate production

Acidosis

Stimulates respiratory drive

Increases the respiratory rate

Figure 6:Increase in Respiratory Rate


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This increase in Respiratory Rate will occur even though the

arterial oxygen saturation may be normal

Text box 7: Arterial Oxygen Saturation

The decrease in oxygen delivery to the tissues, which results intachypnoea, can be due to problems at any point in the oxygen deliverychain (oxygen delivery = cardiac output x arterial oxygen content).

A fall in arterial saturation can be one of the problems; however therecan be falling oxygen delivery despitenormal arterial oxygen saturation(see text box 7). Therefore respiration rate is a more sensitiveindicator of early patient deterioration, and an important vital sign.

Examination

Assessing breathing is the second priority ABC.Again, the look, listen, feel approach is the most sensible.

Look: respiratory rate is one of the most useful signs ofbreathing compromise, as explained above (see text box 8)Look for signs of inadequate breathing:

a) use of accessory musclesb) sweatingc) central cyanosisd) abdominal breathing

e) shallow breathingf) unequal chest movement

Listen: listening first from the end of the bed, for rattlingbreathing (can indicate airway secretions), upper airway stridoror wheeze (partial airway obstruction)(inspiratory orexpiratory).


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Auscultate with a stethoscope to assess depth and equality ofbreathing, and quality of breath sounds.

a) absent or reduced sounds could indicate a pneumothorax

or pleural fluid or collapsed lungb) bronchial breathing indicates consolidation Feel: generally done prior to auscultation

a) palpate position of trachea in suprasternal notch(deviation to one side indicates mediastinal shift, e.g. dueto pneumothorax [away], pleural fluid, lung collapse[towards] or lung fibrosis)

b) palpate chest wall for subcutaneous emphysema or

crepitus (suggestive of a pneumothorax until provenotherwise)

c) assess depth and equality of chest wall movementbilaterally

d) percussion (hyper-resonance suggests pneumothorax;dullness suggests consolidation or pleural fluid)

MET criteria RR< 5 or > 36Text box 8: Respiratory Rate MET criteria

The respiratory rate and arterial oxygen saturations score (see table 3)for the MEWS are as follows:

MEWS 3 2 1 0 1 2 3

Resp Rate < 8 9-20 21-30 31-35 >36

SpO2 % < 84 85-89 90-92 >93Table 3: Respiratory MEWS

Management

Specific treatment will depend on the cause, and it is vital to diagnoseand treat life-threatening conditions promptly, e.g. tensionpneumothorax, acute pulmonary oedema and acute asthma.


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All deteriorating patients should receive oxygen, before progressing toany further assessment. In acute respiratory failure, the aim is to keepPaO2 as close to 100mmHg as possible, but at least 60mmHg (SaO2 90%)

is essential. In most patients, this can be achieved by sitting themupright, and applying 12-15 litres/min of oxygen via non-rebreather mask(see figure 7). If the patient does not improve they will require anICU review.

In a small subgroup of patients who have Chronic ObstructivePulmonary Disease (COPD) and are CO2 retainers, highconcentrations of oxygen can be disadvantageous by suppressing

their hypoxic drive. However, these patients will also suffer end-organ damage or cardiac arrest if their blood oxygen levels falltoo low. The aim in these patients is to achieve PaO2 of 60mmHg,or saturation of 90% on pulse oximetry. So in a patient with COPDwho has a pCO2 > 60mmHg but is also hypoxic, pO2 < 60mmHg, donot turn the inhaled O2 down. If their pO2 is > 60 mmHg, then youcan turn the inhaled O2 down to maintain SaO2 > 90%

FIGURE 7: Oxygen Flow & Inspired Concentration

Oxygen Delivery Systems

There are many oxygen delivery systems available, which are capable ofdelivering a wide range of oxygen concentrations. Delivery systems areclassified into fixed and variable performance devices.

A. Fixed performance devices: provide gas flow that is sufficient forall the patients minute ventilation requirements. In thesedevices, the inspired oxygen concentration is determined by theoxygen flow rate (see table 4), e.g. the Venturi mask(see figure 8).


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Figure 8:Venturi maskmayohealthcare.com.au

Table 4: Venturi MaskDiluter Colour Diluter setting Suggested oxygen

flow rate (Litres/min)

Blue 24% 3

White 28% 6

Orange 31% 8

Yellow 35% 10

Red 40% 12

Please note that the colours and flow rates vary between companies. Always

read the label.

B. Variable performance devices: do not provide all the gas requiredfor minute ventilation, they entrain aproportion of air in addition

to the oxygen supplied.The inspired oxygen concentration will depend on:

a) oxygen flow rateb) the patients ventilatory pattern (If the patient has a

faster or deeper respiratory rate, their inspired oxygenconcentration will be lower, and thus a higher oxygenflow rate will be required)


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c) the amount of air entrained (increasing rate or depth ofbreathing will alter the inspired oxygen concentration)

These devices include nasal prongs, simple facemasks, partial

rebreathing and non-rebreathing masks.a) Nasal prongs (see figure 9) the dead space of thenasopharynx is used as a reservoir for oxygen, and whenthe patient inspires, entrained air mixes with thereservoir air, effectively enriching the inspired gas.Oxygen flow rates of 2 - 4 L/min.

Figure 9: Nasal prongsmayohealthcare.com.au

b) Hudson facemask (see figure 10) reservoir volume ofoxygen is increased above that achieved by thenasopharynx (see text box 9), thus higher oxygen

concentration can be achieved in inspired gas (max 50-60%).

Oxygen flow rates less than 6L/min for Hudsons mask shouldnot be used due to carbon dioxide retention in the mask.

Text box 9: Hudson mask


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Figure 10: Hudson mask

mayohealthcare.com.au

c) Non-rebreathing mask (see figure 11) simple facemask

with the addition of a reservoir bag, with one or two-wayvalves over the exhalation ports which prevent exhaledgas entering the reservoir bag (permits inspired oxygenconcentration up to 95%). Oxygen flow rate of 12-15L/min.

Figure 11: Non-rebreather mask

mayohealthcare.com.au

Monitoring Oxygen Therapy

Oxygen therapy can be monitored clinically (patients colour, respiratoryrate, respiratory distress), using pulse oximetry or arterial blood gases.The advantage of measuring arterial blood gases is that they measureboth oxygen, carbon dioxide levels and metabolic status (includinglactate).


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If the carbon dioxide levels rise in someone with acute respiratoryfailure, it can be a sign that they are tiring and may require ventilatory

support. If CO2 begins to rise in a patient with COPD, it may be prudentto reduce the inspired oxygen concentration, however always rememberthat the arterial oxygen tension should not be allowed to fall below pO260mmHg.

Patients do not die from raised CO2 alone: they die from hypoxaemia,(see text box 10) the eventual consequence of which will be myocardialischaemia, cerebral injury and cardiac arrest.

When taking arterial blood gases, do not remove oxygen mask.It is unnecessary, and may precipitate sudden deterioration.

Text box 10: Arterial blood gases

As long as the concentration ofoxygen being delivered is recorded, thedegree of hypoxaemia can be calculated using the alveolar-air equation &A-a gradient (see text box 11). The blood gas machine will calculate thisfor you (as long as the correct inspired oxygen concentration isrecorded).

Text box 11: PaO2calculation

Pulse oximetry monitors how well the haemoglobin is saturated withoxygen (arterial oxygen saturation). It uses a probe, which shines lightof two wavelengths through the tissues, and detects that which passes

PAO2 = FIO2 PaCO2/0.8

PAO2 should be close to PaO2 in normal lungs


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through. Oxygenated and deoxygenated haemoglobin absorb differentamounts of light, and this information is integrated to determine thearterial saturation.

Oximeters can be unreliable in certain circumstances (see text box 12),e.g. if peripheral circulation is poor, environment is cold, arrhythmias, orif the patient is convulsing or shivering.

If the pulse oximeter does not give a reading, do not assume it isbrokenthe patient may have poor perfusion!

Text box 12: Pulse oximetry

Although pulse oximetry provides excellent monitoring of oxygenation, itdoes not measure the adequacy of ventilation, as carbon dioxide levelsare not measured (see text box 13). This can only be determined byarterial blood gas sampling.

Therefore saturation may be normal but the pCO2 may be highwhich reflects inadequate minute ventilation and hence respiratoryfailure.

Arterial oxygen saturation being normal does not rule out acuterespiratory failure.

Text box 13: Respiratory failure

When assessing a patient remember to incorporate all the vitals

signs, do not just look at an individual reading (see text box 14).

Also remember to think about where they sit in Oxygen Delivery

Chain (see figure 11).


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Remember to incorporate all the vital signs in your assessment!

Text box 14: Vital signs

Airway Breathing CirculationExhaled Air

(CO2, 40 mmHg)

Air (21% O2, 159 mmHg)

Airway obstruction Neuromuscular

Physical: intrinsic central

extrinsic peripheral

Decreased GCS Pulmonary

acute

chronic

Figure 11:ABC-Oxygen Delivery Chain

Heart

andlungs


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SUMMARY

In rare cases, an airway obstruction may be due to mechanical

factors, which are not so easily treated, e.g. airway swelling, post-operative haematoma, infection. This is a medical emergency. ACode Blue/MET should be called.

An increase in Respiratory Rate will occur even though the arterialoxygen saturation may be normal

MET criteria RR< 5 or > 36 In a small subgroup of patients who have Chronic Obstructive

Pulmonary Disease (COPD) and are CO2 retainers, high

concentrations of oxygen can be disadvantageous by suppressingtheir hypoxic drive. However, these patients will also suffer end-organ damage or cardiac arrest if their blood oxygen levels fall toolow. The aim in these patients is to achieve PaO2 of 60mmHg, orsaturation of 90% on pulse oximetry. So in a patient with COPD whohas a pCO2 > 60mmHg but is also hypoxic, pO2 < 60mmHg, do not turnthe inhaled O2 down. If their pO2 is > 60 mmHg, then you can turnthe inhaled O

2down to maintain SaO

2> 90%

Oxygen flow rates less than 6L/min for Hudsons mask should not beused due to carbon dioxide retention in the mask.

When taking arterial blood gases, do not remove oxygen mask. It isunnecessary, and may precipitate sudden deterioration.

If the pulse oximeter does not give a reading, do not assume it isbrokenthe patient may have poor perfusion!

Saturation may be normal but the pCO2 may be high, which

reflects inadequate minute ventilation and hence respiratoryfailure.

Arterial oxygen saturation being normal does not rule out acuterespiratory failure.



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Circulation


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Circulation

Learning Objectives

To understand why pulse rate and blood pressure are vitalsigns and the importance of measuring them

To describe the mechanisms which generate blood pressure, andbe able to define, describe causes of, consequences of andcompensation for hypotension

To understand what is meant by shock To manage hypotension in the deteriorating patient

The Importance of OxygenOxygen reaching the cells and mitochondria is dependent upon adequateoxygen delivery (see figure 12). Oxygen deliverys key components are:

Cardiac output (Stroke Volume x Heart rate)

Arterial oxygen content (Haemoglobin concentration x ArterialOxygen Saturation)

Oxygen delivery = Cardiac output x Arterial Oxygen Content

Stroke Volume HR Hb SaO2Figure 12: Oxygen delivery


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BLOOD PRESSURE

Blood Pressure, Pulse and Oxygen Delivery

Blood pressure (see text box 15) is the product of cardiac output andtotal peripheral resistance (TPR)

Blood Pressure = Cardiac Output x Peripheral Vascular Resistance

Text box 15: Blood pressure

Decreased blood pressure can reflect decreased cardiacoutput and hence decreases the amount of oxygen getting tothe tissues.

Increasedheart rate can reflect a decreasedstroke volume,which may reflect a decreased cardiac output and hence

inadequate amounts of oxygen getting to the tissues. Hence, the measurement of pulse and blood pressure is an

important surrogate marker of whether there is adequatecardiac output and hence oxygen delivery to the tissues andtheir survival (see text box 16).

High pulse and low blood pressure may reflect low oxygen delivery

Text box 16: Low oxygen delivery


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Blood pressure and maintenance of organ function

There are some organs that also require an adequate blood

pressure for their optimal function. The brain and kidney aretwo examples of these. The bodys organs adapt over time to a persons normal blood

pressure. If blood pressure is always elevated, e.g. chronichypertension; the brain and kidneys adapt and will alwaysrequire a greater blood pressure in order to function normally.Therefore it is important to know what your patients normalblood pressure was prior to their current illness. There is a

place to record this on their Observation Chart (see table 2),and the MEWS scores are adapted to reflect the patientsnormal blood pressure.

To calculate the MEWS for heart rate see table 5.

MEWS 3 2 1 0 1 2 3

Heart Rate < 40 41-50 51-99 100-110 111-130 >130Table 5: Heart rate MEWS score

To calculate the MEWS for blood pressure see table 2


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Table 2: Blood pressure score

Hypotension

The generally acceptable definition of hypotension is Systolic blood pressure of less than 100mmHg (see text box

17)

A drop of more than 20% from normal blood pressure

It is important to remember that someone who is normally

hypertensive may be relatively hypotensive even when theirsystolic blood pressure is above 100mmHg.Do not always use 100mmHg as your CRITICAL Systolic Blood

Pressure cut off!

Text box 17: Blood pressure

Patients Usual Systolic Blood Pressure

Additional Considerations

Usual

SBP190 180 170 160 150 140 130 120 110 100 90 80

200s 0 0 1 1 2 2 2 3 3 4 5 5190s 0 0 0 1 1 1 2 2 3 3 4 4

180s 0 0 0 0 0 1 1 2 2 3 3 4

170s 1 0 0 0 0 1 1 2 2 3 3 3

160s 1 1 0 0 0 0 0 1 1 2 2 2

150s 1 1 1 0 0 0 0 0 1 1 2 2

140s 2 1 1 1 0 0 0 0 0 1 1 1

130s 2 2 1 1 0 0 0 0 0 0 0 1

120s 2 2 2 1 1 0 0 0 0 0 0 0

110s 3 2 2 2 1 1 0 0 0 0 0 0100s 3 3 3 2 2 2 1 1 0 0 0 0

90s 4 3 3 3 2 2 2 2 1 1 0 0

80s MET 2 1 0Current

Blood

Pressure

70sMET 4 MET 3

MET 1


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Possible Causes of Hypotension

If blood pressure is the product of cardiac output and total peripheral

resistance, blood pressure can either fall because of;A. a fall in cardiac output orB. a fall in peripheral vascular resistance.

It is important to understand how cardiac output and total peripheralresistance are affected by certain factors.

A.Cardiac outputCardiac output is the product of stroke volume and heart rate (i.e.

flow is the volume per unit time)Factors affecting stroke volume:

1) ContractilityThe ability of the heart to contract in the absence of anychanges in preload or afterload i.e. it is the power of thecardiac muscle.Major negative influences include:

Myocardial ischaemiaAcidosisNegative inotropes (beta-blockers, anti-dysrhythmic)

Major stimulating influences include:Sympathetic nervous systemSympathomimietics (noradrenaline, adrenaline)Calcium

Digoxin

2) Pre-LoadHow well filled is the heart at the end of filling (diastole)?i.e. the end diastolic volume.Increases in end diastolic volume will result in increases instroke volume. There does reach a point that if the end


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diastolic volume over-stretches the heart muscle, the strokevolume can start to decrease.

The major effect of pre-load is venous return to the heart,which is influenced by:a. Intravascular blood volume

Absolute:

Decreases in intravascular blood volume (bleeding,electrolyte and water loss [diarrhoea, vomiting],water loss [diabetes insipidus]) will cause a decrease invenous return and hence a decrease in stroke volume

(see text box 18).Relative:

There is no loss of intravascular blood volume butwith vasodilatation and pooling of blood (vasodilators,epidurals, sepsis) will cause a decrease in venous returnto the heart and hence a decrease in stroke volume.

Decreases in intravascular blood volume can decrease cardiac outputand therefore decrease blood pressure.

Text 18: Intravascular blood volume

b. Intrathoracic pressureIncreases in intrathoracic pressure (asthmatic

attacks, positive pressure ventilation) willrestrict the amount of blood returning to theheart and therefore reduce stroke volume (see textbox 19).


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Increases in intrathoracic pressure can decrease cardiac outputand therefore decrease blood pressure.

Text box 19: Intrathoracic pressure

c. Balance of vasoconstriction and vasodilatation in thevenous system

3) After-LoadThis is the resistance to ejection of blood from the

ventricle.This resistance can either be caused by an outflowresistance from the heart (aortic stenosis) or resistance toflow in the systemic circulation. This resistance isdetermined by the diameter of the arterioles and per-capillary sphincters. As resistance rises, stroke volume isreduced (see text box 20).

Increase in peripheral vascular resistance can decreaseCardiac Output and hence oxygen delivery

Text box 20: Total peripheral resistance

B. Heart Rate:This is determined by the rate of spontaneous depolarisation atthe sinoatrial node. The rate can be modified by the autonomicnervous system:

Parasympathetic stimulation: SLOWS the heart ratevia the vagus nerve e.g. vasovagals, Muscarinicantagonists e.g.: atropine


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Sympathetic stimulation: QUICKENS the heart ratevia the sympathetic cardiac fibres e.g.: stressresponse, temperature

Sympathomemetics e.g.: adrenaline, noradrenaline,isoprenaline

In the absence of conduction through the atrioventricular node(Complete Heart Block), the ventricle will only contract at itsintrinsic rate of 30-40 beats per minute.

Any changes in heart rate, can change the cardiac output. A

faster heart rate can increase the cardiac output and thisoften occurs when the stroke volume is falling and anyreductions in heart rate can cause a decrease in cardiac output.

Does a fast heart rate always increase

cardiac output and blood pressure?

There are situations where an increase in heart rate mayreduce the cardiac output because the ventricle does not haveadequate time to fill with blood, reducing the end diastolicvolume and therefore stroke volume. Cardiac output reducesand may cause a drop in blood pressure (see text box 21). Agood example is atrial fibrillation with a rapid ventricularresponse.

Does a slow heart rate always decrease

cardiac output and blood pressure?

Sometimes when the heart slows there may be no reduction incardiac output. As the ventricle has a longer time to fill, theend diastolic volume is increased each beat, stretches the


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myocardial fibres and increases the stroke volume per beat,this may then compensates for the reduction in heart rate.Therefore, there may be no change or even an increase in

cardiac output and blood pressure. A good example of this is avery healthy athlete.

Text box 21: Fall in blood pressure

C. Peripheral Vascular Resistance

Changes in peripheral vascular resistance (the cumulative resistance of

the thousands of arterioles in the body) can increase or decrease bloodpressure.

1) Increase in peripheral vascular resistance Autonomic Nervous System

a) Stimulation of Sympathetic ReceptorsSympathetic stimulation (1) of the arterioles

can cause vasoconstriction and a subsequentincrease in blood pressure. This often occurs inresponse to a fall in blood pressure (perhaps as aresult of falling cardiac output), which isdetected by baroreceptors situated in thecarotid sinus and aortic arch, reducing thedischarge from them to the vasomotor centre

Fall in blood pressure can reflect: Fall in cardiac output

o Fall in stroke volume due to- Decreased contractility (heart muscle)- Decreased preload (volume)

- Increased afterloado Fall in Heart Rate e.g. Complete Heart Block

Fall in Peripheral Vascular Resistance (PVR)


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with a resultant increase in sympatheticdischarge.e.g. Sympathomimetics that stimulate the 1

receptor will cause vasoconstriction of arteriole,examples include noradrenaline, adrenaline.b) Direct action on arteriole smooth muscle.

Examples include metaraminol, methylene blue,vasopressin, angiotensin.

2) Decrease in peripheral vascular resistancea. Blockade of Autonomic Sympathetic Nervous System

Anything that causes a reduction in the sympatheticstimulation of the arterioles will result in vasodilatation,reducing vascular resistance and blood pressure.Influences include, increasing the stimulation of thebaroreceptors from a rise in blood pressure, which causesa reduction in the sympathetic outflow causingvasodilatation.Any drug that blocks the sympathetic nervous system cancause vasodilatation and a fall in blood pressure.Examples include beta blockers.

b. Direct action on arteriole smooth muscleMolecules and drugs can have a direct effect on thevascular smooth muscle in arteriole causing vasodilatationExamples include:

Vasodilating Drugs:Calcium channel blockers, ACE inhibitors, epidurals,

anaesthetic agents, benzodiazepines.

Vasodilating Molecules:Nitric oxide (infection/sepsis)

Vasodilating conditions:Acidosis, increases in temperature


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Compensatory Mechanisms for Hypotension

An adequate blood pressure is important for the function of vital organsincluding the brain, heart and kidneys. Any reduction in blood pressurewill trigger responses to maintain homeostasis. Depending on the causeof the reduction in blood pressure will depend on the compensatoryresponse.

A. Reduction in Cardiac Output due to1) Reduction in Stroke Volume

Response : There will be a compensatory increase in heart rate

(tachycardia) and a compensatory increase in peripheralvascular resistance (cool, blue peripheries).

If the compensation is effective, blood pressure can bereturned to normal but there will still be the signs oftachycardia and cool peripheries and evidence of

inadequate oxygen delivery because the cardiac outputhas not been restored and therefore it is likely thatoxygen delivery has not been restored (see text box 22).

Clinical Features of a reduction in Stroke Volume:

Reduction in Pre-Load:

Hypotension with a postural drop, tachycardia and cool,blue peripheries

Reduction in Contractility:

Hypotension, tachycardia and cool, blue peripheries withsigns of heart failure

Text box 22: reduction in stroke volume


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2) Reduction in Cardiac Output due to Reduction in Heart RateThere will be an attempt to increase stroke volume and increasetotal peripheral resistance.

Response: Hypotension, bradycardia and cool, blue peripheries.

B. Reduction in peripheral vascular resistance

Response: With a fall in total peripheral resistance, there will be a

compensatory mechanism to increase the cardiac output.Increasing the heart rate usually generates the increase in

cardiac output.

Text box 23: Total peripheral resistance

Consequences of Hypotension

The greatest concern is that hypotension may suggest that

there is an inadequate amount of oxygen getting to the tissues,

which is described as SHOCK.

BLOOD PRESSURE =

CARDIAC OUTPUT X PERIPHERAL VASCULAR RESISTANCE

Text box 24: Shock

Clinical Features of a fall in Peripheral Vascular Resistance: Hypotension, tachycardia and warm peripheries


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The following are possible reasons why hypotension may represent

shock (see text box 24):

A.Inadequate Cardiac Output Cardiac output is integral to the amount of oxygen being

delivered to the tissues. If the cardiac output falls, it islikely that oxygen delivery will fall.

If there is inadequate oxygen delivery to the tissues,inadequate amounts of ATP can be generated which is vitalfor cellular function.

This is turn leads to organ failure, lactate formation and

shock.

B. Inadequate Pressure Gradient Clearly without a pressure gradient across the vasculature

(from high pressure to low pressure) there can be no flow ofblood and its constituents including oxygen which is vital forthe generation of ATP and hence life.

Some organs are able to maintain blood flow through organsdespite changes in blood pressure (autoregulation) eg: brainand kidney. However, there reaches a point when this can nolonger occur if the blood pressure is too low and this in turnreduces blood flow and hence the amount of oxygen reachingthe tissues.

Inadequate blood flow to the organs results in inadequateoxygen delivery to the organs resulting in reducedgeneration of ATP and the formation of lactate. This willlead to organ failure (oliguria and altered mentation), lactateformation and shock.


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When is hypotension not shock?

In order to demonstrate that there is shock there needs to beevidence that organs are failing and/or that there is evidence ofanaerobic respiration by the presence of lactate.

For example: If a patient is hypotensive post anaesthetic and has

warm hands (suggesting good flow to the hands i.e. good cardiac

output), is not confused, has a good urine output with no signs of

heart or respiratory failure and no lactate is found, then the

patient is currently not shocked. However, in these situations it isimportant to continue regular monitoring of the vital signs and

continually look out for evidence of organ failure.

Can a patient with normal or high blood pressure have shock?

The key components to adequate oxygen getting to the tissues arecardiac output and arterial oxygen content. Only if either of thesetwo are reduced can this result in a fall in oxygen getting to thetissues and result in shock. Sometimes, the compensatorymechanisms for a drop in cardiac output, increase in totalperipheral resistance, can result in there being a normal or evenhigh blood pressure measurement. So, despite there being anormal blood pressure, there are signs of organ failure and

anaerobic respiration i.e. the patient is shocked with a seeminglynormal blood pressure.

For example: An elderly lady presents with an inferior myocardial

infarction and complete heart block. On examination she has navy

blue fingers, a heart rate of 40 beats per minute, her blood

pressure is 210/100 mmHg and she has evidence of pulmonary


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oedema and oliguria. Her lactate measurement was 10mmol/L

(normal < 2 mmol/L). So, despite a high blood pressure due to an

enormous increase in vascular tone to try and compensate for the

fall in cardiac output and blood pressure, there is evidence of notonly organ failure but also anaerobic respiration. This patient IS

shocked despite the high blood pressure.

Messages: A patient can be hypotensive even when the systolic blood

pressure is above 100mmHg because their normal blood

pressure is high. Hypotension is a marker of a deteriorating patient and at

risk of increased risk of death Hypotension may mean the patient is shocked but there

needs to be evidence of organs failing due to inadequateoxygen getting to them

A patient can be shocked with a normal or even high blood

pressure

Text box 25: Messages


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The Initial Management of Hypotension

It is important to remember what generates a blood pressure:

Cardiac Output (stroke volume x heart rate) Peripheral Vascular Resistance

It is important to decide from history and clinical examination, which ofthese two has decreased leading to a fall in blood pressure.

A SYSTOLIC BLOOD PRESSURE OF LESS THAN 90mmHg

REQUIRES A CODE BLUE (MET REFERRAL).

A. Fall in peripheral vascular resistance (common causes include

infection, and vasodilating drugs)

History: Chills, fever, symptoms of infection,ingestion/inhalation of vasodilators.

Examination: Signs of infections, usually accompanied bywarm hands (a vasodilated vasculature) and tachycardia.There may be signs of organ failure (confused, oliguria,respiratory failure).

Laboratory Investigations:

Evidence of infection (rise or significant fall in white cellcount)

Evidence of renal dysfunction (rising creatinine) Evidence of lactate formation (metabolic acidosis on

arterial blood gas sampling, lactate rising)


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Management Plan In the absence of tachycardia, organ failure, lactate

formation

If there is no evidence of organ failure (not oliguric,not confused) and no evidence of anaerobic respiration(lactate formation) and no associated tachycardia i.e. lookswell from the end of the bed. Then there may be no need todo anything other than closely monitor the vital signs(hourly measurements, or according to MEWS triggered)over the next six hours to ensure that there is no downwardtrend of blood pressure.

In the presence of tachycardia, but absence of organ

failure and lactate formation

The tachycardia could be in response to a fall in venousreturn (due to pooling in the vasculature) and fall instroke volume that has not affected the amount ofoxygen going to the tissues yet. It is important toimprove venous return and stroke volume to maintainadequate cardiac output and oxygen delivery to thetissues:

o Administer intravenous fluid bolus (20-30 mls/kg or250 mls Normal Saline)

o Continue to perform frequent vital signs to documentany trends (e.g. 1/2hrly for 1 hr, followed by hourlyfor 4 hours, then subsequently 4-hourly if stable)

o If there is an improvement in tachycardia and bloodpressure, then the fluid bolus has been adequate torestore venous return.

o If the tachycardia remains repeat the fluid challengeo Continue to observe responseo If the patient continues to have hypotension,

tachycardia and warm hands, further fluid can be


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administered particularly if there are no signs ofheart failure

o An intensive care review should be requested once

three litres of fluid have been administered and thetachycardia and hypotension are still present.

Hypotension and evidence of organ failure

o Administer intravenous fluid bolus (20-30 mls/kg or250 mls Normal Saline)

o Continue to perform frequent vital signs to documentany trends (1/2hrly x 1 hr, 1/24 x 4, then 4/24 if

stable)o If there is an improvement in tachycardia and blood

pressure, then the fluid bolus has been adequate torestore venous return.

o If the tachycardia, hypotension and organ failureremains, repeat the fluid challenge

o Call for an intensive care reviewo A maximum of three litres of fluid should be

administered before an intensive care review.o Continue to perform hourly observations to ensure

that the trend of blood pressure, pulse and mentalstate are being monitored.

B. Fall in Cardiac Output

There are two predominant common causes of fall in cardiac output,

both having very different presentations: Fall in Pre-Load (common causes include bleeding, loss of fluids and

electrolytes).o History

Will describe histories relevant to bleeding, loss offluid and electrolytes [diarrhoea, vomiting, polyuria


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from hyperglycaemia], loss of water [diabetesinsipidus].

Can also describe symptoms of postural hypotension

(feels faint when standing up, has actually fainted).o Examination

Signs that are relevant to the fluid lost (bleedinginto drains, maelena, nasogastric losses)

Cool, blue hands, tachycardia, hypotension with apostural drop (drops more than 10mmHg from lyingto sitting)

o Laboratory Investigations

Evidence of bleeding (fall in haemoglobin) Evidence of renal dysfunction (rising creatinine) Evidence of lactate formation (metabolic acidosis on

arterial blood gas sampling [negative base excess],lactate rising)

o Management Correct cause of loss of fluid (call surgeon for

ongoing bleeding, may need to correct coagulopathy) Replace whatever fluid has been lost (blood if

bleeding, saline if gut losses, 5% Glucose if diabetesinsipidus)

Estimate how much has been lost by looking at thefluid balance chart, how much is in the drains, howfar has the haemoglobin fallen

In the first instance rapidly administer 500 mls via a

blood pump set through a large bore cannula Observe response (tachycardia should be reduced

and blood pressure increase) Continue to administer fluid rapidly until there is the

desired response:Blood pressure returning to normalHeart rate returning to normal


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o Management If the patient is hypotensive and has signs of organ

failure including heart failure (cardiogenic shock),

the patient will require inotropic support andreferral to either the coronary care unit or intensivecare unit

Stop all intravenous fluids as the patient is bydefinition fluid overloaded

When assessing a patient remember to incorporate all the vitals

signs not just look at an individual reading. Also remember to thinkabout where they sit in the Oxygen Delivery Chain (see figure 13).

Airway Breathing CirculationExhaled Air(CO2, 40 mmHg)

Air (21% O2, 159 mmHg)

Primary Cardiac

Pulmonary circulation

Hypovolemia (sepsis, anaphylaxis)

Figure 13: Oxygen Delivery chain

Heart

and

lungs


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Summary

Blood Pressure = Cardiac Output x Peripheral Vascular Resistance High pulse and low blood pressure may reflect low oxygen delivery It is important to remember that someone who is normally

hypertensive may be relatively hypotensive even when theirsystolic blood pressure is above 100mmHg.

Do not always use 100mmHg as your CRITICAL Systolic Blood

Pressure cut off!

Decreases in intravascular blood volume can decrease cardiacoutput and therefore decrease blood pressure. Increases in intrathoracic pressure can decrease cardiac output

and therefore decrease blood pressure. Increase in peripheral vascular resistance can decrease cardiac

output and hence oxygen delivery The greatest concern is that hypotension may suggest that

there is an inadequate amount of oxygen getting to the

tissues, which is described as SHOCK. Hypotension and warm hands:

Administer fluids Hypotension, cool hands, no signs of heart failure:

Administer fluids Hypotension, cold hands, signs of heart failure:

Cease fluids

Refer to CCU/ICU for inotropes Remember to incorporate all the vital signs in your assessment!

A SYSTOLIC BLOOD PRESSURE OF LESS THAN 90mmHg

REQUIRES A CODE BLUE (MET REFERRAL).


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Central Nervous

System &

Urine Output


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Central Nervous System (CNS)

Learning Objectives: Identify common causes of depressed level of consciousness

(LOC) Describe how to assess a patients level of consciousness Describe how to manage a patient with depressed level of

consciousness

INTRODUCTION

Depressed level of consciousness is a common finding in acute illness.It can occur due to intracranial disease or as a result of systemic insults(see table 6).

Table 6: Common causes of decreased level of consciousness

Intracranial disease Meningitis, encephalitis

Epilepsy

Cerebrovascular disease, SAH

Head injury

CNS infection

Systemic conditions Hypoxia, hypercapniaHypotension, hypo/hyperosmolar

Hypoglycaemia, hyponatraemia

Hypo/hyperthermia

Hypothyroidism, hypopituitarism, Addisons

Sedative drugs

Hepatic encephalopathy, uraemic encephalopathy


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Assessment of CNS function is an important indicator of adequacy of

tissue oxygenationcalled end-organ function. Thus CNS assessmentis included in MEWS.

CNS depression in itself can also be associated with life-threateningcomplications. The most important complication is the associatedinability to maintain an adequate airway. Loss of gag or cough reflex isassociated with a high risk of aspiration.

OXYGEN

Neurones in the central nervous system, like all other cells in thebody, are highly dependent on oxygen. Adequate oxygenation allowsthe formation of large amounts of ATP energy packets which arerequired for all cellular functions (see figure 14).


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1Glucose

Glucose-6-Phosphate

CYTOPLASM

2Pyruvate




NADH NAD ++

H+ + O2 H20

ADP + Pi3P 36ATP

Figure 14: AEROBIC METABOLISM (i.e. with oxygen)

MITOCHONDRIA


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When oxygen supply is inadequate, insufficient ATP is produced (seefigure 15), which leads to failure of some cellular functions. This

causes the symptoms of confusion or depressed level of consciousness.

1Glucose

Glucose-6-Phosphate

CYTOPLASM

2Pyruvate


3Pyruvate Acetyl CoA +2ATP


Figure 15: ANAEROBIC METABOLISM (i.e. in the absence of oxygen)

MITOCHONDRIA

LACTATE


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Oxygen supplies to the cells in the brain depend on the same factorsas oxygen supply to all other tissues in the body (see text box 26).

Oxygen delivery = cardiac output x arterial oxygen content

SV HR Hb SaO2

Text box 26: Oxygen delivery

Thus confusion or decreased LOC can reflectA. decreased cardiac output

o decreased stroke volumeo decreased heart rate

(This may be indicated by a decreased blood pressure)B. decreased arterial oxygen content

o decreased haemoglobin

o decreased arterial saturation


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GLUCOSE

Cells require a substrate in order to form pyruvate, which enters theKrebs in the mitochondria to produce ATP. Many cells in the body canuse glucose, fats or proteins as substrates for energy production.

However neurones are obligate glucose users, and cannot use fats orproteins as substrates in mitochondrial metabolism. Therefore ifserum glucose levels fall too low, neurones will stop producing adequate

amounts of ATP, and cellular function will stop.

Thus confusion or depressed level of consciousness could also resultfrom hypoglycaemia (see text box 27).

Checking the BGL is one of the first things, which should bechecked on an unconscious, or fitting patient, whether they arediabetic or not.

Text box 27: BGL

ASSESSMENT of CNS

A. Level of consciousnessThe sedation score used in the MEWS observation chart, scores the

level of sedation according to the criteria in Table 7 and should bedone on every patient. A sedation score is based on how conscious thepatient is at the time all their vital signs are measured. Dependingon their level of consciousness, a MEWS score for sedation (see textbox 28) is then recorded. This is added to the other MEWS scoresfor other vital signs, and the total score is calculated to give an overallMEWS.


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MEWS 3 2 1 0 1 2 3

SedationScore

0-1 2 3 4

Table 7: CNS MEWS

Text box 28: Sedation score

As outlined above, level of consciousness is an important indicator ofend organ function which is altered by changing amounts of oxygendelivery to the cells.

Another common method of measuring CNS function is the GlasgowComa Scale. This should be done when prescribed by a medicalofficer, attended to as per hospital policy or nursing practice

standards such as unit specific nursing practice standards, or initiatedand attended to if the nurse delivering care deems it appropriate.

Patients with GCS


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best verbal response, and best eye-opening response (see table 8).

Text box 29: MET for LOC

GCS

MOTOR obeys commands 6localises to pain 5

withdraws to pain 4

abnormal flexion to pain 3

extension to pain 2

no response to pain 1

VERBAL oriented 5

confused 4inappropriate words 3

incomprehensible sounds 2

nil 1

EYE spontaneous 4

to speech 3

to pain 2

nil 1Table 8: GCS

B. Pupillary SizeA change in the size, equality or reactivity of the patients pupils is animportant clinical sign. They should be checked when requested by

If there is a sudden fall in consciousness, or a fall in GCS >2

a MET call is indicated


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medical staff, as part of neurological observations, and when there isany reduction in the patients level of consciousness. This can provide

important diagnostic clues (see text box 30).

Pupils can be bilaterally dilated in- sympathetic overactivity, e.g. fear, stress, anxiety, hypoglycaemia- sympathomimetic administration, e.g. overdose of tricyclic

antidepressants, or administration of adrenaline in an arrestsituation

Pupils can be bilaterally constricted when opioids have beenadministered...pinpoint pupils.

Previous surgery or cataracts can affect baseline pupil size and reaction.

Text box 30:Pupil size

MANAGEMENT

1. check airway and breathing; ensure airway is patent head tilt, jaw thrust Guedels or nasopharyngeal airway

2. give high-flow oxygen3. MET call if patient meets the criteria (GCS fallen >2 points)4. if respiratory rate or arterial oxygen saturation is decreased,

may need ventilatory assistance using self-inflating bag & mask5. ensure intravenous access; intravenous fluid bolus may be

required if patient is hypotensive6. reverse any drug-induced CNS depression, e.g. naloxone for

opiod overdose7. measure blood glucose, and correct if


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8. if the airway is patent, and the patient is breathing, placepatient horizontally in lateral recovery position

Once again remember to always incorporate all the vital signs in yourassessment (see text box 31).

Text box 31: Vital signs



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URINE OUTPUT

At the end of this section you will be able to: Identify causes of decreased urine output Identify when to be concerned about low urine output Describe the management for oliguria

INTRODUCTION

Poor urine output is one of the most common triggers for patientreview. It is another end-organ, thus poor urine output can be anindicator of patient deterioration due to many different causes, and isoften one of the earliest signs of overall decline. It is important thatthe causeof poor urine output is correctly diagnosed.

PATHOPHYSIOLOGY

Normal urine flow requiresi. adequate oxygenation of the kidneysii. adequate perfusion pressureiii. normal function of kidneysiv. no obstruction to urine flow, e.g. prostatomegaly, renal calculus,

blocked catheter

Perfusion Pressure

Renal blood flow is autoregulated (i.e. kept constant) throughout awide range of mean arterial pressures (MAP) (70-170mmHg). MAP isthe perfusion pressure seen by the organs (see figure 16 & 17). Thisrange is increased in chronically hypertensive patients, who thenrequire higher blood pressures to maintain normal kidney function.


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Figure 16: Mean arterial pressure

i P

Diastolic BP

120

80

MAP

Systole i e

Figure 17:Mean Arterial Pressure Diagram

If mean arterial blood pressure falls below the lower limit ofautoregulation, renal perfusion pressure will decrease and thus urineoutput will fall.

Oxygen Delivery

In order to function, renal cells require adequate oxygen delivery, justas all the other cells in the body. Oxygen delivery depends on cardiacoutput and arterial oxygen content (see text box 31).

MAP = (2 x Diastolic BP) + Systolic BP3


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Text box 31: Oxygen delivery

If oxygen delivery falls to the kidney, urine output will fall. If oxygendelivery is insufficient for renal function, it reflects inadequate

oxygen delivery to other tissues as well. Therefore urine output canbe a sensitive sign of the adequacy of whole-body oxygen delivery.The MEWS score for urine output is calculated using table 9.

MEWS 3 2 1 0 1 2 3

Urine for

4 hrs (mls)

800

Table 9: MEWS for urine output

MANAGEMENT

Need to first diagnose the cause of decreased urine output.? decreased renal blood flow in the face of decreased bloodpressure, cardiac output or tissue oxygen delivery? obstructed urine flow needs to be urgently corrected if

this is the case, thus it is important to diagnose early (seetext box 31 & 32)

Urine output should be > 0.5 mls/kg/hr i.e. 35mls/hr for a 70 kg person

Text box 31: urine output


SV HR Hb SaO2


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Decreased Renal Blood Flow

This can be due to decrease in Cardiac Output, as a result of Decreased stroke volume

o Decreased pre-loado Decreased contractilityo Decreased after-load

Alteration in heart rate

Change in peripheral vascular resistance

There is a small window of opportunity for reversingoliguria and preventing acute renal failure.

Text box 32: oliguria

When oliguria is due to decreased perfusion i.e. decreased blood

pressure or cardiac output, it is potentially reversible. In thiscircumstance, the most important initial management is to excludehypovolaemia (decrease in cardiac preload) being the cause. Ifhypovolaemia is likely (relative or absolute) give an intravenous fluidbolus of 25-50mL/kg. Frusemide is not to be given unless you haveruled out all other possible reasons for low urine output, and thepatient is clinically fluid overloaded (see text box 33)


SV HR [Hb] SaO2

Figure 17: Oxygen delivery


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Giving a fluid bolus will increase circulating volume, thus increasepreload, and ultimately increase cardiac output. This will result in

increased blood pressure, increased renal perfusion pressure, andultimately increase the patients urine output.

Obstruction

Absolute anuria should be seen as a sign of urinary tract obstructionuntil proven otherwise.- assess bladder size

- check catheter patency- if there is no catheter in-situ, the patient may need one inserted

Do NOT give Frusemide to oliguric patients unless you

have ruled out all other possible reasons for low urine

output, and the patient is clinically fluid overloaded.

Text box 33: Frusemide

Again remember to incorporate all the

vital signs in your assessment!


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Summary

Figure 18: ABC

In order to have adequate oxygen delivery to the tissue all three

areas of Airway, Breathing, and Circulation must be functioning

well. If there is an alteration in one section the body will try to

compensate for the reduced oxygen delivery. This will be evidentin the alteration in vital signs. If the body is unable to

compensate, then deterioration occurs which will ultimately result

in organ failure.


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SUMMARY

Checking the BGL is one of the first things, which should bechecked on an unconscious, or fitting patient, whether they arediabetic or not.

If there is a sudden fall in consciousness, or a fall in GCS >2 aMET call is indicated

Remember to incorporate all the vital signs in your

assessment!

Urine output should be > 0.5 mls/kg/hr i.e. 35mls/hr for a 70kg person There is a small window of opportunity for reversing oliguria

and preventing acute renal failure. Do NOT give Frusemide to oliguric patients unless you have

ruled out all other possible reasons for low urine output,

and the patient is clinically fluid overloaded.


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Communication,

Team Work andManagement Plans


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Communication, Team Work and Management Plans

One of the most important factors in determining an acutely illpatients outcome is the quality of the communication of the teaminvolved.

In each team, each member has their strengths and weaknesses,varying skills and different levels of knowledge. The art of managingthe deteriorating patient is determining the role of each member of

the team, identifying their comfort zones and working together in thisknowledge to affect the best outcome for the management of theparticular patient. The steps for optimising the management areoutlined in text box 34. The flowchart in figure 19 gives you a basicoutline for management.

Optimising the management of the sick patientrequires:

1. Gathering as much information as possible

2. Integrating this information into the presentation of the

patient

3. Communicating any concerns about a patient to other

members of the team

4. Addressing each team members concerns or respond

adequately5. Formulating, documenting and communicating a

management plan with a provisional diagnosis

6. Actioning the management plan

7. Reassessment for possible re-review and escalation

of the management plan

Text box 34: Optimising management


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Figure 19: Flow chart

1. Gathering Information

Each member of the team provides vital information about thepatients course in hospital and all of this information must beintegrated to inform our assessments, decisions and subsequentactions.

For example:

1. A nurse who has been caring for a patient who is deterioratingwill convey significant information about the patients cognitive

state both pre and post event to a medical officer who has

reviewed a patient for the first time. This may significantly

alter the doctors interpretation of what is wrong with the

patient in the acute setting.


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2. The team physio may have noticed that a patients exercisetolerance or arterial oxygen saturations on exercise havesignificantly deteriorated. This may alert the team to lower

respiratory tract infections or perhaps even pulmonary emboli.

This should be communicated and documented in the notes.

It is important in the management of the deteriorating patient, togather as much information from different members of the team as

possible. See text box 35 for sources of information.

This can be obtained from: Verbal contact with members of the team Reading the daily notes from each different member Reviewing observation, fluid charts, and medication

charts Comparing current presentation with previous

presentations

Text box 35: Sources of information

2. Integration of Information

The next step is to integrate the information they have gathered tobetter understand the current situation of the patient. e.g.- the needto understand why a BP has fallen or why a heart rate or respiratoryrate has risen. Please refer to each individual section on vital signs forfurther information.


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3. Communicating Information

Once information has been gathered and thought has been given towhat is going on, the next step is working out what to do with theinformation! This obviously depends on each individuals level ofknowledge and understanding. If an enrolled nurse finds an abnormalarterial oxygen saturation, they may refer that information to theregistered nurse who is working with them for more guidance aboutwhat to do. If an RMO is concerned by a deteriorating patient, then

they need to discuss these findings with their registrar and possiblyconsultant. As text box 36 highlights you must ensure that thepatient is being attended appropriately.

The important thing is to recognise when there is an

abnormality in vital signs and make sure someone more senior

knows about it and that someone is attending the patient

appropriately!

Text box 36: Abnormalities and appropriate care

When communicating about a high MEWS, also communicate whatobservations has triggered the MEWS (e.g. MEWS 4 due to Pulse 102,RR 26, Temp 38.7). For a person to be able to appropriately triage andadvise on a particular patient, they need to actually know theparameters that have caused the score rather than just a number. Wemust remember that each member of the team needs to prioritise andattend to many things.This means we have to:

identify that there is a problem attempt to interpret the problem in the context of the

patient we are caring for

then communicate this to the appropriate people for actioning.


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SBAR CommunicationThe SBAR technique is an easy, structured, and useful tool to helpcommunicate concerns, and call for help or action.

SBAR1 stands for Situation, Background, Assessment andRecommendation (see text box 37).

Situation: What is the current situation, concerns,observations, MEWS, etc

Background: What is the relevant background. Thishelps set the scene to interpret the situation aboveaccurately.

Assessment:What do you think the problem is? This isoften the hardest part for medical people. This requiresthe interpretation of the situation and backgroundinformation to make an educated conclusion about what isgoing on.

Recommendation: What do you need them to do? Whatdo you recommend should be done to correct the currentsituation?

Text box 37: SBAR


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For example:

A 75-year-old lady with a history of IHD is admitted with a

fractured neck of femur. Twelve hours post-operatively, she

complains of chest pain and her arterial oxygen saturation has

fallen to 78% on 2L nasal prongs. You as the person nursing

her are concerned that she is acutely unwell and needs

attention. If you wish to use the SBAR communication

technique you would say something like this:

SITUATION

I have an elderly lady who has dropped her arterial oxygen

saturations and is complaining of chest pain

BACKGROUND

She is twelve hours post-op for a fractured neck of femur

and she has a history of ischaemic heart disease

ASSESSMENT

She has a MEWS of 4, her saturations have dropped to 88%,

and she is tachycardic at 112. I think she is acutely unwell and

may have

In this case she may have a pulmonary embolus, a myocardial

infarction or even just pneumonia. If you are not sure what isgoing on then you can just say that you thinks she is unwell.

RECOMMENDATION

I think this patient may be having a MI and they need an ECG,

some S/L GTN (anginine) and more oxygen with an urgent

medical review.


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You have effectively communicated the reason you are calling,

given the person some background information that may help

them in identifying the cause of the situation, given them anidea of how sick you think the patient is and identified that

you feel the patient needs review.

In the worst case scenario if you are not getting the attention thatyou think this patient deserves or you are not sure what to do next,then you can end with This a significant change in the medical status

of the patient and this patient needs a medical review urgently.

Documenting Problem/Communication

Once you have you actioned a particular problem, you always mustdocument what you have done. This may involve documenting lowarterial oxygen saturations, and that you have contacted a doctor, orif you are medical officer what treatment you have advised. This

documentation has a two-fold purpose.

It helps the flow of information from one shift to the nextand often helps to clarify your own thought processes.

This is also a medico legal requirement.

You must always identify who needs to know about a deterioratingpatient, communicate as much as possible, and document appropriately(see text box 38).


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When communicating information you must:

1. Identify who the most appropriate

person is to inform when you encounter a

deteriorating patient.

2. Communicate as much information as

possible to the next in line to ensure thatthey have all the information needed to

appropriately triage and advise on the

situation. Use the SBAR tool!

3. Document the steps you have taken to

remedy the situation and actions taken.

Text box 38: Communicating

4. Adequate response to information/concerns

After being involved in the management of a deteriorating patient,many people feel that things could have been done better. It might bethat they felt the root of the problem was not being addressed andsomething else was going on, or that they just felt that theirparticular views were not taken into account. Each member of theteam has different priorities with respect to patient management andthese need to be integrated into the management plan.

After communicating with more senior colleagues, an individual mayfeel as if they were not taken seriously or their particular concernabout a situation wasnt addressed. This can be remedied by

specifically asking each member of the team what their concerns are,


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how they think this can be addressed, and integrating those concernsinto their management plan.

Sometimes people looking after a patient are not sure what anabnormal result means. They feel worried about ringing someone, asthey are afraid they might seem stupid or even get scolded for notknowing. This behaviour does not help anyone and there are variouscommunication tools that you can use to overcome this.

For example:

A nurse is told to take the blood pressure in the left and right

arm for a person with central chest pain. However, this

particular patient may have a fistula or have had a mastectomy

and cannot have bilateral blood pressure measurements

performed. The doctor comes back to review all the collected

information and review the management plan only to find out

this has not been done. If the doctor had specifically asked ifthe nurse had any problems with the plan, the issue would have

been identified much earlier, saving everyone time and allowing

the appropriate observations to be measured in a timely

fashion.

The primary responsibility of the doctor is to stabilise the

patient. However, the needs of the ward and the nursing staffneed to be integrated into this plan. The nursing staff may

feel that the patient cannot be managed in a general ward

because of level of nursing care required, but the doctor feels

that there is no medical reason that they need step up of their

care. This needs to be discussed and a plan endorsed by all

members, and agreed on.


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Theoretically, in the event of a deteriorating patient (for example at a

MET call), all people involved in the patient should be present. SBARshould be used for communicating during MET calls as well (see textbox 39).

Use the SBAR strategy when communicating at a MET call as well

Text box 39: SBAR

It is the job of the team leader to voice their concerns, pre-emptother peoples concerns and integrate that into their management plan.By simply asking what are peoples main concerns the team saves time.Often issues are raised that had not been considered and if all teammembers feel as if their concerns are validated, in the end it benefitsthe patients care.

5. Formulating, Documenting and Communicating Management Plans

The make or break of patient care is often in the formulation ofmanagement plans. To allow successful flow of information from oneteam, one shift and one ward to the next, plans MUST be documented(see text boxes 40 and 41). They must be thorough, yet concise andmost importantly understandable (both legible and logical!).

Optimal management plans include action plans for all members of theteam and time frames in which things must be actioned. Medical staffmust always document their impression, that is the provisionaldiagnosis (see text box 42).


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When documenting a medical entry always document:H-historyE-examinationI-impression/diagnosisP-management plan

Text box 40: Documentation

Management Plans should include:a) Observation ordersb) Nursing ordersc) Allied health ordersd) Change in therapy orderse) Investigation/intervention ordersf) Notification orders

Text box 41: Management plans

When this is done, each member has a clear idea of their roles andresponsibilities and no excuses for not following them!

Medical Staff-Alwaysdocument your impression, i.e. the provisional orworking diagnosis

a) Observation Orders

Often change in frequency of observations being performed areneeded, for example a person with a blood pressure falling from

150/90 to 98/50 after review, may need their frequency of


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observations changed so that vital signs are done every half an houruntil the blood pressure is above a certain level and stable without

intervention.

b) Nursing Orders

More intensive monitoring may be needed if a patient deteriorates, forexample changing the bag of an IDC from a free drainage to an hourlymeasure bag to monitor urine output more closely.

c) Allied Health Orders

An example of an allied health order is a person who has

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