Introduction to the Management of Critical Ill Patient

KURSUS CRITICAL CARE

HOSPITAL SERDANG

Definition Of Critically Patient

• Critically ill patients: Decompensation of the status of the patient leading

without therapeutic intervention to the multiorgans failure and to the death

• Critically ill patients: Those patients who are at high risk for actual or potential

life-threatening health problems. The more critically ill the patient is, the more likely he or

she is to be highly vulnerable, unstable and complex, thereby requiring intense and vigilant nursing care.

Every Critically Ill Patients are constantly in EMERGENCY OR RED ALERT condition.

Potentially to advance to life threatening event such as cardiac or pulmonary event.

THUS

Active Treatment and Prevention including closed monitoring, fast and correct actions are mandatory.

Number of Admission into ICU/HDW, Hospital Serdang

2006 2007 2008

ICU 307 407 461

HDW - - 624

(Mei – Dis)

PESAKIT KRITIKAL

TRAUMA & BURN

SEVERE INFECTION & SEPTICAEMIAi. Pneumoniaii. Diabetic Footiii. Peritonitisiv. Meningitis

UNCONTROL MEDICAL PROBLEMi. DKAii. CVAiii. Renal Failureiv. Acute Br. Asthma

AMI & HEART FAILURE

MAJOR OPERATION

Trauma Infection

Postoperative

Tumour

Head injury

Shock & Hypotension

Uncontrol Chronic Disease

Metabolism disorder

Pulmonary embolism

Causes

Which organ systems are most commonly involved in critically ill patients?

• Respiratory System• Cardiovascular system• Internal or Metabolic environment• Central Nervous System• Gastrointestinal Tract

AIM OF ASSESSMENT

1. Identify the physiologically abnormalities

2. Identify the most appropriate way to correct the abnormalities

3. Diagnose the underlying problem

History taking, examination and initial resuscitation often occurring simultaneously.

Overview Of The Systems Function

Tissue &Capillary

O2CO2

Blood With Low Oxygen Content, High CO2 Content

Blood with High Oxygen Content, Low CO2 Content

Gas Exchange: i. In the lung: between alveolar and blood in pulmonary circulation ii. In the tissue: between cells in tissue & blood in systemic circulation

Respiratory Cardiovascular

In Normal Condition:The Circulation System willCarry the blood all over the body

O2

CO2

Glucose + O2 → CO2 + H2O + E

CO2O2

At the Tissue

At the Lungs

In Normal Condition: The Cellular Respiration happened in the cytoplasma and proceed into the mitochondria. This process need O2 (Aerobic metabolism)

In Abnormal condition when the CVS and Respiratory System function reduced, the systems failed to supply O2 to the cells foraerobic metabolism. The cells will go into anarobic metabolism.This lead to organs failure and production of lactate(lactic acid).

Effects of Hypoxia

• Aerobic metabolism at the Cytochrome oxidase system is replaced by anaerobic metabolism ( increased lactate production)

• Membrane pumps cease functioning; irriversible cell damage may follow.

• Brain & heart function reduced (most susceptible). Followed by other organs if prolonged.

• Critical value of O2 at mitochondrial level is 1 mmHg.

What system should be evaluated first?

• First few minutes of evaluation should address life-threatening physiologic abnormalities.

• Usually involving the airway, the respiratory system, or the cardiovascular system.

• Then the evaluation should expand to include all organ system

• ABC of resuscitation

How is vital organ perfusion assessed?

The vital organs & their method of initial evaluation are as follows:

Skin : assess warmth, capillary refill in all extremities.

CNS : assess level of consciousness & orientation.

Heart : measure BP & HR, ask for symptoms of myocardial ischemia (eg., chest pain)

Kidneys : measure urine outputLungs : (as slides before)

Warning Signs of a Severely Ill Patient

• Blood pressure : SBP <90 or mean < 70 mmHg• Heart rate : > 150 or < 50 bpm• Respiratory rate : > 30 or < 8 breaths/min• Conscious level : GCS < 12• Oliguria : < 0.5 ml/kg/hr• Sodium : < 120 or > 150 mmol/l• Potassium : < 2.5 0r > 6 mmol/l• pH : < 7.2• PaO2 : < 94%• PaCO2 : < 35 mmol/L and > 45 mmol/L• Bicarbonate : <18 mmol/l

Arterial Blood Gas

• pH : 7.35 – 7.45• PaO2 : > 60 mmHq• PaCO2 : 35 – 45 mmHq• SaO2 : 90% - 100%• Standard Bicarbonat : 21 – 27 mmol/L• Actual Bicarbonate : 23 -25 mmol/L• Base Excess (BE) : -5 – 5• Lactate : 0.4 – 1.4 mmol/l

Step 1: Look at pH - this is the starting point. If within normal range, a normal or compensated state exists. If outside normal

limits, assess whether acidosis or alkalosis is present. The body never overcompensates. Whichever state exists on the pH scale is the primary abnormality.

Step 2: Assess hypoxemic state. If PaO2 is <60 mmHg, hypoxic state exists. If PaO2 is between 80 -100 mmHg, a normal condition exists. If PaO2 is >100 mmHg, a hyperoxic state exists.

Step 3: Assess ventilatory status. If PaCO2 is <35 mmHg, it is termed "alkalosis" (alveolar hyperventilation or hypocarbia). If PaCO2 is between 35-45 mmHg, it is within normal limits. If PaCO2 is >45 mmHg, it is termed "acidosis" (ventilatory failure or hypercarbia). If possible, determine whether this is an acute or chronic state (see the compensation explanation).

Step 4: Assess metabolic component. 1. If bicarbonate (HCO3-) is <22 mEq/l, it is termed "acidosis". 2. If bicarbonate is between 22-28 mEq/l, it is within normal limits. 3. If bicarbonate is >28 mEq/l, it is termed "alkalosis". 4. If possible, determine whether this is an acute or chronic state

ABG : Interpretation Guidelines

Arterial Blood Gas Disturbances in acid-base balance

Respiratory Phatology

• Respiratory acidosis (that is, ventilatory failure) the drop in pH is explained by the change in PaCO2

• Respiratory alkalosis (that is, alveolar hyperventilation) the decreased PaCO2 explains the increased pH

Metabolic Phatology

• Metabolic acidosis reduced pH not explained by increased PaCO2. It is usually associated with an increased anion gap due to the accumulation of renal acids, lactic acids, and ketoacids (from diabetes or starvation)

• Metabolic alkalosis raised pH out of proportion to changes in PaCO2. It is associated with hypokalaemia, volume contraction, or exogenous alkali administration

Groups of patients who are difficult to assess

Young adults Compensatory mechanisms tend to mask signs of severe illness until the illness is very advanced’ Significant physiological abnormalities in these patient therefore indicate very severe illness

Elderly or immuno-compromised pt

The inflammatory response may be damped, again hiding signs of severe illness. In addition the physiological reserve of these patients is often severely compromised.

Trauma patients

Difficult to assess due the multitude of possible injuries & the effect of the distracting pain making injuries difficult to localize. Detailed mechanism of injury very useful

Subsequent Assessment

REVIEW

- on going review of response to treatment

- plan for subsequent management

ACUTE RESPIRATORY

FAILURE

CAUSE OF RESPIRATORY FAILURE

What is the Diagnosis ?

CAUSE OF RESPIRATORY FAILURE

Definition

Hypoxemic respiratory failure (type I) is present when the arterial partial pressure of oxygen (PaO2) is <8 kPa (60 mmHg) when the patient is breathing room air.

Hypercapnic respiratory failure (type II) is present when the arterial partial pressure of CO2 (PaCO2) is > 6.7 kPa (50 mmg).

Disorders that initially causes hypoxemia may be complicated by respiratory pump failure and hypercapnia.

Definition

Diseases that produce respiratory pump failure are frequently complicated by hypoxemia resulting from secondary pulmonary parenchymal processes (eg. pneumonia) or vascular disorders (eg. pulmonary embolism)

Disorders that initially causes hypoxemia may be complicated by respiratory pump failure and hypercapnia.

Signs And Symptoms of Resp. Failure

Dyspnea, Tachypnea, Gasping

Used of Respiratory Accessory muscle

Kaussmal’s Breathing

Cyanosis

Hypertension (early) Hypotension (later)

Tachycardia (early) Bradycardia (later)

Reduce Sensorium and Concious level.

Poor Arterial Blood Gaseous (ABG) reading

Type Of Respiratory Failure

Respiratory Failure Type I:• PaO2 < 60 mmHq (hypoxia)• PaCO2 < 40 mmHq * Hyperventilating when PaCO₂< 35 mmHq.

Respiratory Failure type II:• PaO2 < 60 mmHq.• PaCO2 > 45 mmHq (Hypercarbia)

* Hypoventilating

Causes

Pulmonary Causes• Pneumonia• Bronchitis• Emphysema• Pneumothorax• Lung Contusion• Pulmonary Oedema• Lung Collaps

Extrapulmonary causes• Airway obstruction• Diaghpragm Pathology And

Phrenic nerve palsy/paralyse

• Neuromuscular disease: Myasthenia Gravis & Guillain’s Barre

• Ribs Fracture• Cervical bone fracture (esp.

above C3)• Septicaemia• Severely Blood loss

This will lead to hypoventilationand hypoxia

Causes of Respiratory Failure

1. Low inspired partial pressure of oxygen

2. Hypoventilation

3. Ventilation perfusion mismatch

4. Diffusion abnormality

Common causes of breathlessness based on speed of onset

minutes hours Days-weeks

Pneumothorax

Pulmonary embolism

Pulmonary oedema

Asthma

Pneumonia

Pulmonary oedema

Metabolic acidosis

Pleural effusion

Exacerbation of COPD

pneumonia

Bronchial tissue: Edema, Inflammed & hyperamia: Br. Smooth muscle contraction

Bronchial lumen narrowed

Increased sputum& mucus production

Effect Of Infectioni. Cough reflexii. Resp. Muscle activityiii. Cilia Functioniv. Bronchial smooth muscle contraction

Cross Section Of Airway During Infection: Bronchitis

Abnormal Bronchi

Normal Bronchi

Bronchial Asthma

Management Of Respiratory Failure

Oxygen Therapy

Chest Physio&

Sputum mobilisation

Nursing Care Antibiotic

Bronchodilator

Chest Physio & Sputum MobilisationEncourage sputum clearance: : chest physio : encourage cough and regular tracheal suction : Humidifier & sputum diluents drugs

Spontaneous breathing and cough movement help to reduce respiratory muscle atrophy.

Humidifier and sputum diluents drug help: : to dilute the sputum/mucus : reduce and prevent cilia dysfunction : Remember: O2 gas is a dry and cold gas. It need

to be humidified

Bronchodilator

Action: Reduced bronchoedema. Reduced mucus secretion. Bronchial smooth muscle relaxationCan be given through: Nebuliser, Inhaler, Intravenous, Oral and

Subcutaneous.Group: -2 stimulant (Terbutaline) Anticholinergic (Atrovent®) Aminophyline (theophyline®)

Bronchodilator

C.Physio Bronchodilator

C.PhysioDilated Bronchi,Sputum still present

Clearance Of sputum

Sputum clear up,Bronchi still narrow

Bronchial dilatation

Effect Of Broncho dilator& Chest physio

Nursing care

Very important.

Patient in prop up position.

: Reduce the effect of splinting abdomen

: Increased respiratory effort and reduced work of breathing

: Reduced atelectasis (lung unit collapes) especially at the lower zone.

: Easy to cough.

It help to reduce the complications such as Bed sore, DVT and Nosocomial infection.

Oxygen Therapy

• O2 is widely used across all medical specialities

• It is life saving & part of first line treatment in many acute critical situations

• It should always be considered along with mx of the airway, breathing, circulation, constant monitoring and reassesment of treatment.

• Method of O2 delivery is part of this mx.

When O2 therapy indicated?

• Cardiac and respiratory arrest (give 100% O2)

• Hypoxaemia ( PaO2<60mmHg, SaO2<90% )• Systemic hypotension ( SBP<100mmHg )• Low COP & metab.acidosis ( HCO3¯

<18mmol/L)• Resp.distress ( RR>24/min )• In anaesthesia ( during & after )• Septicaemia

Prescribing oxygen:controlled or uncontrolled?

• As with any drug, O2 should be prescribed.

• Most pts benefit from uncontrolled O2

• However a small group COAD patients requires controlled O2 therapy (used Ventimask).

They depend on hypoxia drive to stimulate respiration These pts should received carefully controlled O2

therapy, starting at 24 - 28%, which is progressively increased.

Aiming to achieve a PaO2 > 50mmHg or SpO2 of 85 - 92%.

Oxgen Delivery System

Water bath Humidifier Without Humidifier

Oxygen Flowmeter

Pin Index Flow meter& Oxygen Pressure regulator

Bull Nose Flow meter& Oxygen PressureRegulator

Oxygen Delivery Devices

2 main types of devices :

• Fixed performance devices pt receives a constant inspired O2 concentration

(fix FiO2) despite any changes in minute ventilation

• Variable performance devices the O2 conc. delivered is variable depending on

pts minute ventilation (pts effort), O2 flow rate & peak inspire flow rate.

VentiMask

Adjustable oxygenConcentrationDelivery system

Fixed performance devices

Variable Performance Devices

• Nasal cannula• Simple face mask• Trachaemask• High flow mask• Head box

Oxygen flow must be adequate to prevent rebreathing of carbon dioxide

Variable Performance Devices

Method Of Oxygen therapy

Nasal Pronged

Face mask

Ventimask

High Flow Mask

Mechanical Vent.

O₂Flow > 5 L/m (FiO2 35%-70%)

FiO₂: 24%- 60%

O₂Flow > 10 L/m

O₂Flow < 4 L/m (FiO2 24%-36%)

Inadequate flow can cause rebreathing and hypercarbia

Progress Of Oxygen therapy

Nasal Pronged

Face mask

Ventimask

High Flow Mask

Mechanical Vent.

SpO2 & PaO2 worseningInspite O2 therapy

Worsening of other Vital signs in spite of Mx.: BP: Tachycardia/ bradycardia: PaCO2: GCS : persistence tachypnoe/dyspnea

Wean Of Oxygen therapy

Nasal Pronged

Face mask

Ventimask

High Flow Mask

Mechanical Vent.

SpO2 & PaO2 beter With O2 therapy

Improving of other Vital signs & optimisation of Mx.: BP : HR normalised: PaCO2 normalised: GCS improved: tachypnoe/dyspnea stop.

Danger of Respiratory Failure

Hypoxia: • Brain damage• Cardiac event: AMI,

arrthymias• Acute Renal Failure• Acute Liver Failure

• Death

Hypercarbia :• Stimulation Adrenal

Activity• Acid-base

disturbance: Respiratory Acidosis

• Electrolites imbalance: danger of hyperkalaemia

Effects of Hypoxia

• Aerobic metabolism at the Cytochrome oxidase system is replaced by anaerobic metabolism ( increased lactate production)

• Membrane pumps cease functioning; irriversible cell damage may follow.

• Brain & heart most susceptible.Followed by other organs if prolonged.

• Critical value of O2 at mitochondrial level is 1 mmHg.

Low inspired partial pressure of Oxygen

• High altitude

• Inadvertent oxygen disconnection on a patient receiving oxygen

Hypoventilation

1. Respiratory center depression- drug ingestion, anaesthesia, head injury, encephalopathy, fatigue etc

2. Disruption of respiratory signal during transmission along the nerves to the respiratory muscles- spinal injury, motor neurone disease, Guillain-Barre syndrome

3. Dysfunction of the neuro-muscular junction- paralytic agents, myasthenia gravis

4. Dysfunction of the muscles of respiration- myopathy, fatigue, malnutrition, dystrophy

5. Chest wall abnormalities- kyphoscoliosis, ankylosing spondylitis, pleural fibrosis

Ventilation perfusion mismatch

1. Physiological shunting

- pneumonia, pulmonary oedema, pulmonary haemorrhage and contusion, atelectasis

2. Anatomical shunting

-intracardiac shunting (eg. Fallot’s tetralogy, Eisenmenger syndrome)

3. Increased physiologic dead space

- hypovolemia, pulmonary embolus, poor cardiac function, or high intrathoracic pressures ( from positive pressure ventilation)

Diffusion abnormality

• The alveolar and capillary distand increased d/t interstitel infiltrate or fluid in the alveolar sac.

• Thus the gasseos (O2 and CO2) difficult to travel.

• Common in Pneumonia pulmonary oedema & ARDS

• Severe destructive disease of the lung – late fibrosing diseases,

Respiratory Monitoring

1. Clinicala. Increased work of breathing :

tachypnea, use of accessory respiratory muscles, nasal flaring, intercostal/suprasternal/supraclavicular retraction, or a paradoxical breathing.

b. Sweatingc. Tachycardiad. Hypertension (hypotension and

bradycardia are late signs)e. Altered mental status- ranging

from agitation to coma and seizures

f. Cyanosis – central and peripheral

2. Arterial blood gases

3. Pulse oximetry- Extremely useful monitor- Estimates arterial saturation- The relationship between saturation

and PaO2 is described by Oxyhemoglobin Dissociation Curve

- Desaturation ~94% is critical threshold because below this level a small fall in PaO2 produces sharp fall in SpO2.

- Conversely, a rise in an arterial PaO2 has little effect on saturation.

- The main determinant of O2 content of blood and O2 delivery to tissues is the SATURATION, not the PaO2.

4. Capnography

60 100 PaO2 (mmHq)

90

100

SaO2(%)

Oxygen Dissociation Curve

40

40

SaO2 above than: 90%Small increased in SaO2 Large increased in PaO2

THUSFalls in PaO2 may be

Tolerated well

SaO2 below than : 90%Large dropped in SaO2Small dropped in PaO2

THUSReduced the Oxygen

Content

Oxygen Content /100 ml blood = 1.34 x Hb (g/%) x SaO2 + 0.03 x PaO2 (mmHq)

94

70

SaO2

PaO2SaO2

PaO2

Lower alarm limit

• Pulse oximetry

- common source of error is poor peripheral perfusion which will lead to a discrepancy between the heart rate displayed by the pulse oximetry and HR measure by the ECG

- other sources of error : bilirubine pigments, false nails or nail varnish, bright ambient light, poorly adherent probe, excessive motion, methaemoglobin & carboxyhemoglobin.

Management Principles

• Must correct the hypoxemia• If uncorrected, FATAL• Rapid reversal of hypoxemia is obviously critical• Hypoxemia should be treated by oxygen

supplementation (increase FiO2) or increase mean airway pressure ( mechanical ventilation)

• Risk of oxygen induced hypoventilation in hypercarbic patients with an acute exacerbation of COPD is low.

Thank you