Recognition and Treatment of

the Critically Unwell PatientRebeka Wright PA-R, BSc (Hons), PgDip (Physician Associate studies), PGCert (Critical Care)Physician Associate Critical Care – Guys and St Thomas’ Hospital NHS Foundation Trust

No conflict of interests

Introduction

History of critical care

Recognising the unwell

patient

Respiratory failure

Shock

Renal Failure

Correcting abnormal

physiology in first instance

diagnostic considerations

second

Many simple interventions to

correct abnormal

physiology can occur in

ward setting

Critical Care

“care for patients who have potentially

recoverable conditions who can benefit from

more detailed observation ( with or without invasive treatments) then can be provided safely

in an ordinary ward”. Intensive Care Society

Level 2 – single organ failure, post op, stepdown

from higher levels

Level 3 – advanced respiratory support alone of

monitoring or support two or more organ systems

History of Critical Care Florence Nightingale in her observation of recovery areas near the

operating theatre

1923 – Johns Hopkins Hospital USA – post op neurosurgical patients

WWII and Korean and Vietnam wars

Modern concept after Poli epidemic in 1952 Copenhagen positive pressure ventilation from ‘iron lung’

Further expansion in 1960s

1992 First formation of advisory committee for intensive care medicine

2001 First ICM training programme launched

2010 Faculty of ICM training

Very heterogeneous – variable care nationwide

Recognising the Unwell

Patient

Essential to recognise to

initiate immediate action to

correct abnormal physiology

Anticipation of at risk patients

e.g. post op

ABCDE approach

NEWS2 >5 review by clinician

with critical care experience, >7 MET call/peri-arrest

Airway

Airway obstruction

Impaired airway protection

Breathing

Respiratory arrest RR<8 or >25

SaO2 <90%/paO2 <8Kpa on 50%

FiO2

pCO2 >6.5 or pH <7.3

HR <40 or >130

Lactate >2 BE >-4

UOP <0.5ml/kg/hr

GCS <12 or drop >2

Prolonged siezures

NEWS2

NEWS2

NEWS2

Monitoring

Other equipment

Respiratory Failure

Key Concepts

Causes

Oxygen therapy

HFNC

CPAP

NIV

Invasive Ventilation

VV- ECMO

Key Concepts SaO2 indicator of oxygenation NOT ventilation.

Average person at rest 1L/min TV supply metabolic

demands – we breathe more for CO2 clearance

Minute Ventilation = Tidal Volume (TV) x RR – pCO2

is inversely proportional to MV

Simplified alveolar gas equation

PAO2 = FiO2 (Patm –pH2O) – PACO2/R~0.8

• simply the more CO2 there is the less space there is

for O2

Dead space – 2ml/Kg – part of each breath that

does not take part in gas exchange – anatomical

and alveolar

VA (alveolar volume) = RR x (TV – dead space)

V/Q matching – West Zones

Optimal V/Q = 1

PPV increases

zone 2

V/Q 0.36

Causes respiratory Failure

1. Acute Hypoxaemic – Type 1 pO2 <8 normal or

low pCO2

V/Q mismatching – Pneumonia, PE, pulmonary

oedema, ARDS

2. Ventilatory – Type 2 raised pCO2 >6.5-7

CNS depression, respiratory muscle weakness

3. Post – Op – atelectasis and reduction FRV

4. Type IV respiratory failure – hypoperfusion or

shock.

DO2 = CO x CaO2 = [(Hb x SaO2 x k) + (PaO2 x

0.023)

Oxygen therapy

Nasal specs, venturi

Oxygen therapy in

hypercapnia

o Causes pulmonary

vasodilatation increases

shunt fraction

o Haldane effect –

deoxygenated Hb high

affinity for O2

o Hypoxic drive

HFNC

CPAP – improved

oxygenation

PEEP

prevents alveolar collapse improving recruitment thus improvement of V/Q mismatching

Decrease in venous return – leading to decrease in preload and

decreased work load

NIV

NIV mask

NIV

BTS guidelines

NIV - non invasive ventilation

Indications – acute hypercapnic respiratory failure

pH <7.25 pCO2>6.5 RR >23 if persisting after bronchodilators and O2

COPD, NM disease/chest wall deformity, OSA/OHS

Contraindications

Absolute – severe facial deformity/burn/upper airway obstruction

Relative pH <7.15 or pH <7.25 + (GCS <8, confused, agitated cognitive

impairment

ICU referral – impending resp arrest, NIV failing to reduce pCO2, SaO2<85% on

NIV, need for sedation to tolerate, pH <7.25 or RR >25 on optimal setting – if fail

NIV then ventilated mortality is increased

Asthma/pneumonia – poor outcomes

Complications – pressure ulcer, gastric distension, PTX

1. Set PC/PS

2. Set

BUR

16-20

3. Set Ti

0.8-1.2

(PC

only

4. IPAP – inspiratory positive airway pressure aid inspiratory

pressure to increase inspiratory pressure – improves PaO2 and

CO2 – 15 (20 if pH <7.25) max 30

5. EPAP – expiratory positive airway

pressure stents upper airways and recruits

underventilated lung – improves PaO2 – 3

unless OSA known or suspected max 8

NIV trouble shooting

Elevated PaCO2 = increase IPAP or decrease EPAP – IPAP – EPAP

= TV and MV is TV xRR

Low PaO2 = increase EPAP/IPAP/both – not home NIV (max FIO2

0.5)

ABG after 30-60mins

Use 24/7 then taper 72hrs

Invasive Ventilation

Invasive ventilation

Indications – RR>35 PaO2 <8

on FiO2 0.5% PaCo2 >7.5 pH

<7.25 GCS <8, poor sputum

clearance, exhaustion,

failure to improve on NIV

RSI – sedative, opiate,

neuromuscular blocker –

preoxygenate-sedative-

NMB-cricoid pressure-

intubation

Cardiovascular response-

Reduces RV preload, LV

afterload

Set up

1. FiO2

2. Mode- Full or partial/ volume or

pressure

3. Full support – RR TV (6ml/Kg) or Pinsp

(to target TV)

4. PEEP

5. I:E

Increase pO2 increase FiO2/PEEP

Decrease pCo2 Increase MV (TV xRR)

VV-ECMO Large bore cannulae venous system through

oxygenator

Allows lungs time to heal

Not haemodynamic support

Rescue method – refractory hypoxaemic respiratory faliure

Potentially reversible aetiology

ShockClinical syndrome when acute circulatory failure

with an inadequate or inappropriately distributed

perfusion results in failure to meet tissue metabolic

demands causing generalized cellular hypoxia

Signs and Symptoms: Confusion, Tachypnoeia,

Hypotension, Cold or cyanosed or warm and

flushed, Decreased UOP

Key concepts

Types

Management

Monitoring

Key Concepts - preload

MAP = CO (SV x HR) x SVR

SV determined by preload, afterload, myocardial contractility

Preload – myocardial sarcomere length prior to contraction – EDV (echo)or EDP ( CVC/PAC)

• Venous return

• Ventricular compliance

• Pericardial compliance

• Valvular disease

• Atrial kick

• Ventricular wall thickness

• Intrathoracic pressure

Key concepts - Afterload

MAP = CO (SV x HR) x SVR

Afterload – sum of the forces opposing

ventricular ejection = Ventricular wall stress

Ventricular wall stress directly proportional to

P x r/ T

P = ventricular transmural pressure (ITP – Ventricular

cavity pressure during ejection)

r = ventricular chamber radius (increased with EDV)

T = Ventricular wall thickness

Key concepts - Contractility

MAP = CO (SV x HR) x SVR

Contractility – factors other than HR, preload and

afterload responsible for changes in myocardial

performance. Primarily dependent on intracellular Ca2+

• Drugs

• Disease – Ischaemia, HF

• Autonomic tone

• Increased HR

• Increased afterload

Types Cardiogenic

• MI and complications

• Myocarditis

• Myocardial contusion

• Takotsubo

• Septic

• Drugs

• Cardiomyopathy

• Dysrhythmias

• Severe AR, AS or MS

• LVOT obstruction

Endocrine/metabolic

• Adrenal insufficiency

• Hypo/hyperthyroid

• DKA

• Severe electrolyte disturbance e.g. low Ca2+

Obstructive

• Massive PE

• Atrial thrombus

• Cardiac tamponade

• Abdominal compartment syndrome

• Tension pneumothorax

• Dynamic hyperinflation – asthma

Hypovolaemic

• Haemorrhage

• Fluid loss

Distributive

• Neurogenic

• Liver failure

• Septic

• Anaphylaxis

Types of Shock

High

Cold

Low

Cardiogenic/obstructive

Septic

Warm

High

Sepsis/ CO2 retention

Fluid overload

Low

Warm

High

Sepsis/anaphylaxis

Cold

Low

Haemorrhage/

Fluid loss

anaphylaxis

Peripheries

Pulse volume

Diagnosis

CVP/JVP

Neurogenic, endocrine

Management Shock

Identify aetiology is key

Correct hypoxaemia

Dependent on aetiology – treat underlying cause

Optimise preload

Minimise Afterload

Increase contractility

Volume resus – optimise preload Bleeding – blood products

Colloid e.g. albumin

Crystalloid – physiologically

balanced

Assessing fluid

responsiveness – straight leg

raise

Increase SVR Vasopressors

• Noradrenaline = alpha

(beta 1)

• Phenylephrine pure alpha

agonist

• Metaraminol = alpha

(beta 1+2)

• Vasopressin V1

Iinocostrictors

• Adrenaline = alpha and

Beta 1 (beta2)

Alpha receptors = peripheral

vasoconstriction

Beta1 receptors =

chronotrophy and inotropy

Beta 2 receptors

vaso/bronchodilatation

MAP = CO (SV x HR) x SVR

Increase contractility Inodilator

• Dobutamine = beta 1, 2

(alpha)

• Levosimensan and

milrinone (PDE)

Inoconstrictor

• Adrenaline alpha and

Beta 1

• Dopamine – low dose D1

vasodilation,

intermediate B agonism,

high dose Alpha agonism

MAP = CO (SV x HR) x SVR

CO monitoring

Sepsis – life threatening organ dysfunction

due to dysregulated host response to infection

SOFA or qSOFA (SBP <100, RR>22 GCS <15) score >2 (mortality 10%)

Septic shock – MAP <65 + Lac>2 despite adequate fluid resuscitation (mortality

>40%)

Management – begin immediately

30ml/Kg crystalloid in 3hrs

Regular review of CO (dynamic over static variables) MAP>65 if req vasopressors

Fluid resus to normalise lactate

Cultures

Abx – broad- spectrum (within 1hr of recognition), rationalised once organism

identified. Not in inflammatory conditions, duration 7-10/7, short duration, PCT

Identification of source and source control

Noradrenaline (need art line), dobutamine

Hb>70, Plt>10 or >20 if risk of bleeding, >50 if bleeding or needing proceedure

Renal Replacement

Threapy

Indications

o Fluid overload (refractory to medical treatment)

o Refractory hyperkalaemia

o Uraemic pericarditis/ encephalopathy

o Refractory metabolic acidosis pH<7.3

o Raised Cr

Types CRRT, PIRRT, IHD

CRRT – haeamodynamic instability

Access

HD – dialysis via diffusion

HF – filtration

mix

Anticoagulant

Exchange rate L/min – Ur/Cr, K

Fluid removal / fluid balance

Questions ?