PRINCIPLE MANAGEMENT

OF ICU PATIENTS
MUHAMMAD FADZLI BIN OSMAN (082019040006)
JULIANA BINTI KAMARUDIN (082019040005)
MUHAMMAD IZZAT HARRAZ BIN ISKANDAR NEEZA (082019040004)
INTENSIVE CARE UNIT
• Refers to care provided in a separate, The patients usually coming to ICU are:
specially-staffed and equipped hospital 1. Respiratory failure and need
unit dedicated to the observation, care mechanical ventilatory support
and treatment of patients with life
threatening illnesses, injuries or 2. Required very high level of monitoring
complications from which recovery is 3. High risk of cardiorespiratory failure
generally possible.
• Total number of beds in ICU should be
10% of hospital beds.
 ACUTE RESPIRATORY FAILURE
• Inability of lungs to maintain adequate oxygenation with or without
acceptable elimination of carbon dioxide.

Type Cause
Type 1 •Po2 <60mg Hg •ARDS
(oxygenation failure) •PAO2 (alveolar)- PaO2 (arterial) gradient increased •COPD
•Increase dead space •Pulmonary edema
•C02 is usually normal or even low •asthma

Type 2 •pO2 normal •Overdosage of narcotics/ barbiturate

(hypercapnic ventilation) •PCO2 >50mmhg /benzodiazepines
•PAO2-paO2 normal •Residual paralysis of muscle relaxant
•Brainstem infarction

Type 3 •ARDS
(combined oxygenation •COPD
and ventilatory failure) •asthma
MANAGEMENT OF RESPIRATORY FAILURE
1. Supplemental Oxygen
• To achieve pO2 of 80mmHg
• Improves all type of hypoxia except histotoxic hypoxia
• Does not fully corrected hypoxia produced by shunt (even 100%
O2)
• Delivered via mask, nasal cannula, venturi mask, T-piece attached
to endotracheal or tracheostomy tube
• Ideally, inspired oxygen concentration (FiO2) should not be >50%:
otherwise oxygen toxicity can occur
MANAGEMENT OF RESPIRATORY FAILURE
• 2. Mechanical ventilation
• Carried out by connecting endotracheal
tube (nasal or oral) or tracheostomy tube
to ventilator
Indication: on the basis Criteria
of
Blood-gas analysis •P02 <50mmHg on room air / <60mmHg on
FiO2
•pH <7.25 (acute RS failure)
•PCO2 >50mmHg
•pO2/Fi)2 < 250mmHg (normal > 400mmHg)
•P(A-a)O2 gradient >350mmHg on 100% O2
Pulmonary function •RR >35/min
•Vital capacity <15mL/Kg
•Dead space volume (vd/vt) >0.6 (60%)
•Peak negative pressure < -20mm H20
•Tidal volume < 5mL/Kg
other •Excessive fatigue of RS muscles
•Loss of protective airway reflex (aspiration)
•Inability to cough adequately
• Ventilators:
Governing factor
Initiation of breath •Assist ventilation: Patient’s Spontaneous
breaths
•Control breath: Ventilator
Sustain of breaths •Preset volume: Fix present tidal volume
is delivered, called as volume targeted/
volume controlled ventilation.
•Preset pressure: ventilator will deliver
till preset pressure is attained, called as
pressure targeted/ pressure controlled
ventilation.
Termination of •Preset volume (expiration starts once
inspiration/ starting of preset tidal volume delivered)
expiraiton •Preset pressure (expiration starts once
preset pressure attained)
MANAGEMENT OF RESPIRATORY FAILURE
• 2. Mechanical ventilation
Initial setting of Ventilator:

Parameters
Tidal volume 6-8 mL/Kg
Respiratory rate 10-12 breaths/min
Inspiratory: expiratory ratio 1:2
Inspiratory flow rate 60-80 liters/min
Trigger sensitivity (sensitivity of ventilator to -1 to -2 cm H2O
detect patient spontaneous breath)

FiO2 (delivered concentration of oxygen) <0.5 (50%). Initially, patient is started with
100% oxygen but should be reduced to <0.5 at
the earliest if patient maintains oxygen
saturation >90%
MANAGEMENT OF RESPIRATORY FAILURE
2. Mechanical Ventilation
• Modes of ventilation
1. Intermittent positive pressure ventilation
(IPPV) / controlled–mode ventilation (CMV)
• Total breathing of the patient is controlled
by ventilator
• Preset tidal volume and respiratory rate
• No spontaneous effort by the patient
• Disadvantage : intrathoracic pressure
always remains positive decreasing the
venous return and cardiac output.
2. Assisted-controlled (A/C) Ventilation
• Assists the patient spontaneous breathing to
preset tidal volume
• Can also deliver control breath if required
• Ventilator breath is initiated by patient
spontaneous breath
3. Synchronized intermittent mandatory
ventilation (SIMV)
• Delivers preset mandatory breaths
• Ventilator delivers between spontaneous
breaths or coincide with inspiration; never
during expiration
MANAGEMENT OF RESPIRATORY FAILURE
4. Inverse Ratio Ventilation (IRV)
• Normal I:E ratio is 1:2. This is reversed to 2:1
• Increase inspiration time will double the gas
exchange time
5. Pressure Support Ventilation (PSV)
• Preset pressure is delivered to each breath
• It decrease the work of breathing
• It overcomes resistance offered by
endotracheal tube and ventilator tubing
• Can be used alone or in combination of
SIMV
6. Proportional- Assisted Ventilation (PAV)
• Similar to PSV, but delivers the required
pressure by calculation of the lung
compliance and not a fixed pressure
7. Pressure-controlled Ventilation (PCV)
• Maintains a constant preset pressure for a
preset time
• Ventilator will cycle to expiration once preset
time is lapsed
• Tidal volume is determined by set inspiratory
flow and inspiratory time
• Prone to hypoventilation but less prone for
barotrauma.
MANAGEMENT OF RESPIRATORY FAILURE
8. Neurally Adjusted Ventilatory Assist (NAVA)
• Diaphragm activity is sensed by a sensor
placed in distal esophagus to trigger
ventilatory breath
10. High-frequency Ventilation
• Applicable in conditions in which adequate tidal
volume cannot be delivered, hence compensated by
high frequency

9. Dual Mode Ventilation 11. High Frequency Positive-pressure Ventilation

• Breath delivered is volume guaranteed and • 60-12-cycles/min
pressure regulated
13. High-frequency Jet Ventilation
• Decrease chances of hypoventilation and
• 100-300 cycles/min with gases at high pressure of
barotrauma
60psi
• Most common: pressure-regulated volume
control (PRVC)
• Mode of choice for ventilation in current day
critical care practice
MANAGEMENT OF RESPIRATORY FAILURE
3. Add on modes/ positive pressure airway
therapy
• Can be used alone or in conjunction with the
mentioned ventilation modes.
II. Continuous-positive airway pressure (CPAP)
• Basically PEEP given to non-intubated patient
• Non invasive
• Given through a tight fitting mask

I. Positive end-expiratory pressure (PEEP)

• Positive pressure is given at the end of
expiration to prevent alveolar collapse
leading to gas exchange even during
expiration
• Useful for: pulmonary edema; ARDS; thoracic
surgeries
III. Bilevel positive airway pressure (BIPAP)
• Positive pressure during both inspiration and
expiration
• Typical setting: 8-20cm H2O (inspiration) & 5
cmH2O (expiration)
• Intubated or non-intubated

• A/e: hypotension, decrease cardiac output,

increase pulmonary artery pressure (PAP);
increase dead space; increase barotrauma
MANAGEMENT OF RESPIRATORY FAILURE
4. Noninvasive positive pressure ventilation Equipment:
(NIPPV) • Tight fitting face mask in acute setting
• Since intubation and tracheostomy carry
• Nasal mask in chronic setting full face mask
high risk of complication, go for NIPPV
and helmet are also option
whenever possible
• Can be given through special CPAP/BIPAP
Candidates for NIPPV Contraindication devices or through ventilators
•Respiratory failure but •Cardiac or respiratory arrest
there is no urgent need of •Sever hypoxemia
intubation •High risk of aspiration
•Conscious and cooperative •Facial trauma
patients •Inability to protect airways
•No risk of aspiration •Upper GI bleed
•Face mask could be tightly
fitted
 MANAGEMENT OF RESPIRATORY FAILURE
4. Noninvasive positive pressure ventilation Complication
(NIPPV) • Leakage: can lead to hypoventilation. Avoided
Protocol and principles for NIPPV by using tight fitting masks.
• Explain the procedure to patient • Patient inconvenience
• Mask should be tight fitting • Claustrophobia (for mask and helmet)
• Preferably keep head end in propped up position
• Increase risk of aspiration
• Usual settings are
• Skin breakdown, facial edema on prolonged use
• Inspiratory pressure (IPAP): 8-2-cm H20
• Expiratory pressure (EPAP): 5-10cm H2O • Delay intubation.
• FiO2: 1.0 to begin with
• Trigger sensitivity: maximum
• Titrate IPAP, EPAP and FiO2 as per tidal volume
and blood gases
• Give a trial for 1-2hours. If no improvement or
deteriorate, intubate. If improve, reassess every 4
hours
MANAGEMENT OF RESPIRATORY FAILURE
5. Weaning from Ventilator (Discontinuing from ventilator)
Method
• Shift from control mode ventilation to assist control and SIMV
• Then keep on decreasing the rate of breath delivered by ventilator gradually till it becomes 1-2
breath/min
• If tidal volume is not sufficient then pressure support ventilation may be instituted.
• The pressure support may be decreased gradually till the patient achieves adequate tidal volume.
• Once patient’s frequency and tidal volume are adequate then ventilator can be disconnected and T
tube is attached to endotracheal tube.
• If patient is able to maintain normal pulmonary and cardiac functions ad shows normal blood gas
analysis for more than two hours, extubation can be attempted.
MANAGEMENT OF RESPIRATORY FAILURE
6. Monitoring 7. Management of Shock

• Pulse rate 8. Nutritional Support

• Blood pressure a) Enteral route: Short term feeding large bore

nasogastric (Ryle’s) tube, but for long term
• ECG
jejunostomy tubes should be used.
• Oxygen saturation
b) Parenteral Route: Used when the enteral
• Respiratory parameters eg: tidal volume, minute route is not possible or is unable to provide
volume, frequency, airway pressure, FiO2 etc sufficient caloric intake.
• CVP 9. Control of Infection/ Secretions
• Urine output 10. Maintenance of other organ functions
• Other special monitoring depends on specific 11. General Nursing care :
indications
• Care of bladder, bowel, intravascular fluid
volume and other organ functions
 PULMONARY EDEMA

Anaesthesiology posting

Juliana binti Kamarudin 082019040005

 Pulmonary edema
Abnormal accumulation of fluid in interstitial and alveolar
spaces of lungs.

Divided into 2 types

1. Hemodynamic type
2. Increased permeability type
 1. Hemodynamic type
 Commonest cause : Left heart failure (cardiogenic edema)
 Pulmonary artery occlusion pressure rises to more than
25mmHg (30 cm 𝐻2 0)

 OTHER CAUSE :
 Excess volume (reperfusion type)
 Sudden expansion of collapsed lung (re-expansion type)
 Decreased oncotic pressure like in hypoalbuminemia
 neurogenic
 1. Hemodynamic type
Treatment of cardiogenic edema
 Propped up position (45degree head elevation)
 Oxygen inhalation
 Morphine
 Remove fluids from lungs by diuretics (furosemide)
 Reduction of preload by nitroglycerin infusion
 Reduction of afterload by sodium nitroprusside infusion
 Improve cardiac output by
- Cardiac glycosides
- Dopamine
- Dobutamine
 Rotating tourniquets
 Treatment of underlying cause
 Oxygenation not improved, patient be taken up for mechanical
ventilation with PEEP
 2. Increased permeability type (non-
cardiogenic)
Adult respiratory distress syndrome (ARDS)
• Increased capillary permeability leading to
pulmonary edema followed by epithelial cell
damage

• Overall mortality in ARDS is 30-40% - due to

multiorgan failure
• Risk factors for increased mortality
 Old age
 Low 𝑃𝑎𝑂2 , 𝐹𝑖𝑂2 ratio
 Septic shock
 High sequential organ failure assessment (SOFA)
score
 Associated comorbidity, renal or liver disease
 2. Increased permeability type (non-
cardiogenic)

Diagnosis of ARDS (Berlin definition)

3 stages of ARDS severity

Mild : 𝑃𝑎𝑂2 /𝐹𝑖𝑂2 ≤ 300 mmHg with PEEP or CPAP ≥ 5cm 𝐻2 0
Moderate : 𝑃𝑎𝑂2 /𝐹𝑖𝑂2 ≤ 200 mmHg with PEEP ≥ 5cm 𝐻2 0
Severe : 𝑃𝑎𝑂2 /𝐹𝑖𝑂2 ≤ 100 mmHg with PEEP ≥ 5cm 𝐻2 0

Other criteria to diagnose ARDS are :

 Onset of respiratory symptoms within 1 week of a known clinical insult
 Bilateral opacities on X-ray chest which are not nodules, effusions, or lung
collapse
 Respiratory failure not explained by cardiac failure or fluid overload
 2. Increased permeability type (non-
cardiogenic)
Causes of ARDS
• Sepsis
• Lung infection
• Pulmonary aspiration
• Polytrauma (shock lung
syndrome)
• Toxins, inhalation of smoke,
fumes, carbon monoxide/dioxide
• Oxygen tocixity
• Pancreatitis, peritonitis
• Drowning
• Anaphylactic reaction
• Radiation pneumonitis
• Acid inhalation
• Thoracic trauma
• Burns
2. Increased permeability type (non-cardiogenic)

Management of ARDS
• Supplemental oxygen (patient able to maintain 𝑝𝑂2 >60mmHg, 𝑝𝐶𝑂2 <50mmHg,
RR <35/min). If not, add CPAP/BIPAP.
• Mechanical ventilation
- Vt <6mL/kg
- Keep plateau airway pressure 𝑃𝑝𝑙𝑡 <30cm 𝐻2 𝑂
- 𝐹𝑖𝑂2 as low as possible
- PEEP of 5-12 cm 𝐻2 𝑂
- Muscle relaxants
• Bronchodilators, antibiotics, mucolytics
• Steroids
• Prone position
• Recruitment manuever
• Treat the underlying cause
Thank you
Intensive Care Management for Chronic
Obstructive Pulmonary Disease (COPD)
Name: Muhammad Izzat Harraz Bin Iskandar Neeza
ID: 082019040004
Learning Outcome
By the end of this presentation, students should be able to:
• Important management of COPD patients
• Acid-base management
• Respiratory Acidosis and Alkalosis
• Metabolic Acidosis and Alkalosis
IMPORTANT MANAGEMENT OF COPD
PATIENTS
• These patients survive on hypoxic drive therefore during oxygen
supplementation – keep low flows (1-2 L/min), otherwise hypoxic
drive may be lost and the patient can go in apnea
• Once put on ventilator, COPD patients are most difficult to be weaned
– maintain oxygenation by noninvasive positive pressure ventilation
(NIPPV) with CPAP/BIPAP
• These patients should be put on ventilator based on clinical
judgement rather than by blood gas reports
• Ventilator setting include small tidal volume, low breath rate (6-
8/min) & longer expiratory time to allow maximum exhalation
• These patients have decreased body resistance – prone for infection –
need for asepsis during any procedure
ACID-BASE MANAGEMENT
• Acid-base disturbances may be respiratory or metabolic based on
arterial pH, partial pressure of CO2 (pCO2)and bicarbonate
level(HCO3-)

HOW TO TAKE BLOOD GAS SAMPLE?

• Arterial sample is taken either from radial artery or femoral artery
• Must be taken from heparinized syringe (glass syringe preferred over plastic
syringe because oxygen can diffuse through plastic), all air should be removed from
syringe and sample to be sent in ice if immediate analysis is not
possible
INTERPRETATION OF NORMAL BLOOD GAS
• pH: 7.35-7.45
• pCO2: 35-45 mmHg
• HCO3-: 24-26 mEq/L
• Base deficit: -3 to +3
• SpO2 (oxygen saturation): 96-98%
• (A-a) DO2(Alveolar to arterial difference): 3 to 5 mmHg
 [HCO3-]
pH = pK + log
[pCO2 x 0.03]
• If normal pH is maintained at 20:1 - The pH may
be normal in spite of acid-base imbalances or in
other words, it can be said that acid-base
abnormalities have been compensated
• To compensate or maintain normal ratio:
- Any increase in pCO2 is associated with increase
in bicarbonate (bicarbonate retention by kidney)
- Any decrease in pCO2 is associated with
decrease in bicarbonate (excess excretion of
bicarbonate by kidneys).
DIAGNOSTIC APPROACH
• Problems in interpretation arise when more than one abnormality
coexist at a time
eg. Respiratory acidosis in COPD patients may be associated with
metabolic acidosis due to decreased cardiac output (cor pulmonale)
and renal flow.
• Acid-base disturbances may be acute (non-compensated) or chronic
(compensated)
• Diagnostic approach: See the pH, pCO2, bicarbonate level (normal,
increased, decreased)
 pH is Decreased (<7.35)
Look for pCO2

Normal pCO2 Increase pCO2 Decrease pCO2

Increased Decreased or
HCO3- is decreased normal HCO3-
Decrease HCO3-
HCO3-

Respiratory Respiratory acidosis +

Metabolic acidosis acidosis Metabolic acidosis Metabolic acidosis
 pH is Increased (>7.35)
Look for pCO2

Increased pCO2 Decreased pCO2

Increased HCO3- Increased HCO3- Decreased HCO3-

Respiratory alkalosis +
Metabolic alkalosis Respiratory alkalosis
Metabolic alkalosis
 pH is Normal (7.35-7.45)
Look for pCO2

Normal pCO2 Increase pCO2 Decrease pCO2

Normal HCO3- Increased HCO3- Decrease HCO3-

No acid-base Chronic metabolic

abnormality Respiratory acidosis + acidosis (due to renal
Metabolic alkalosis disease) and chronic
respiratory alkalosis due
to pulmonary disease
RESPIRATORY ACIDOSIS
• Definition: It is defined as increase in pCO2 sufficient enough to decrease the pH to less
then 7.35

• Causes:
- Hypoventilation which may be because of overdosage of drugs and anesthetics
- Disorders of neuromuscular junction effecting muscles of respiration
- Central CNS depression
- Lung disease eg. COPD
- Excessive CO2 production eg. Malignant hyperthermia

• Treatment:
- Mechanical ventilation; if pCO2 is high (>50 mmHg)
- Acidosis should be treated slowly
- Treatment of underlying cause
RESPIRATORY ALKALOSIS
• Definition: Decrease in pCO2 sufficient to increase the pH to more than 7.45

• Cause: • Treatment:
- Hyperventilation
- Adjustment of ventilator setting (decrease
- Iatrogenic the frequency) and increasing the
- Pregnancy rebreathing eg. Exhaled gases containing
- Salicylate poisoning CO2
- Hypoxia - CO2 inhalation
- CNS trauma - Treat underlying cause
METABOLIC ACIDOSIS
• Definition: Decrease in pH <7.35 / CO2 Normal and HCO3- Decreased
• Cause:
- Renal failure
- Circulatory failure (shock) leading to accumulatio of lactic acid
- Hepatic failure
- Diarrhea with loss of bicarbonate
- Cyanide poisoning
METABOLIC ACIDOSIS contd.
• Treatment:
- Sodium bicarbonate
- Dose can be calculated by formula: Sodium bicarbonate (mEq) = 0.3 x body
weight x base deficit
Half of the calculated dose is to be given immediately and the remaining dose only
after getting the next blood gas analysis report. It is mandatory to have adequate
ventilation before giving sodium bicarbonate because sodium bicarbonate
produces carbon dioxide onmetabolism & can worsen the acidosis.
- Other buffers:
1) Carbicarb (sodium bicarbonate + sodium carbonate): It is a non CO2 generating
alternative to sodium bicarbonate but clinical studies are lacking
2) THAM: Non-sodium containing compound
- Treat the underlying cause
METABOLIC ALKALOSIS
• Definition: Increase in pH >7.45 / Increased CO2 and HCO3-

• Cause:
- Vomiting
- Ryle’s tube aspiration (loss of HCL)
- Diuretics
- Hypovolemia
- Iatrogenic

• Treatment
- Treat underlying cause
- IV infusion of ammonium chloride or 0.1 N hydrochloric acid (not more than 0.2
mEq/kg/hr)
References

• Short textbook of anesthesia, Ajay Yadav, 6th edition

• www.criticalcarepractitioner.com
• www.anesthesiajournal.co.uk
Thank You