This document provides an overview of fundamentals of surgical intensive care. It discusses definitions of intensive care and critical illness, types of surgical ICU patients, scoring systems used in ICUs, hemodynamic monitoring techniques, principles of oxygen delivery and consumption, shock classification and treatment, mechanical ventilation including modes and settings, acid-base abnormalities, complications of ventilation, and conditions like acute lung injury, sepsis, and acute renal failure. Key concepts covered include physiology support, multisystem disease management in critically ill surgical patients.

1. Fundamentals of
Surgical Intensive care
Presented by
Dr.Mohammed Alsiraj
MBBS,MRCS1(Ed),MRCS2(Ed)
Surgery Resident

2. Intensive Care
 Generally refers to the care of
patients who are critically ill or
injured, thereby requiring
 Constant monitoring,
 Frequent assessment and
 Thoughtful intervention
 A thorough understanding of human
physiology and how to support or
correct alterations from the normal
is essential.
 Critical illness often affects the
entire body and a multisystem
approach must be considered.

3. Surgical ICU
 Trauma
 Cardiac surgery
 Transplantation
 Pediatric surgery
 Burns

4. Scoring systems in ICU
 Statistical modelling techniques to
assess patient variables and
prognosticate on patient outcome.
 No scoring system is accurate
enough to predict the outcome of a
given patient.
 APACHE (II,IV)
 SAPS (II,III)
 ISS
 RTS
 MPM
 TISS

5. Haemodynamic monitoring
 Continuous ECG
 Arrhythmia or ischemia
 HR
 Cuff blood pressure:
 Pulse oximetry
 Temperature
 Respiratory rate
 Invasive:
 Arterial catheterization
 Central venous catheterization
 Pulmonary artery catheterization
 Non invasive:
 Doppler ultrasound
 Echocardiography
 Pulse contour analysis

6. Frank-Starling curve
• CO = SV × HR
• SV = EDV − ESV
• CI = CO/BSA
 SVR = (MAP − CVP)/CO
 MAP = DBP + 1/3(SBP − DBP)
 CPP = MAP - ICP

8. Inotropes :
 Inotropes are drugs that work
directly on the heart to increase its
output by increasing the heart rate
and contractility
 cAMP-dependent:
 β-adrenergic agonists
 phosphodiesterase inhibitors
 cAMP-independent:
 α - adrenergic agonists
 digoxin
 Catecholamines:
 Adrenaline
 Nor-adrenaline
 Dopamine
 Dobutamine
 PDI:
 Amrinone,
 Milrinone
 Enoximone
 Digoxin

10. Vasopressors:
 Vasopressors are agents that cause
vasoconstriction of the peripheral
vasculature.
 Their main purpose is to increase
MAP.
 This is done predominantly via α-
adrenergic mechanisms.
 Catecholamines
 Nor-adrenaline
 Phenylephrine
 neurogenic shock

11. Vasoregulatory agents :
 Vasoregulatory agents are
endogenous mediators that have a
role in maintaining vascular tone.
 Vasopressin
 Vasopressin infusions have been
shown to decrease
catecholamine requirements in
patients with septic shock.
 Steroids
 Stress-dose steroids (300 mg
hydrocortisone per day) may
improve vascular responsiveness
to catecholamine infusion in
patients with septic shock.
 This has been a controversial
topic.

12. Intra-aortic balloon pump
(IABP)
 is an invasive device utilized to increase cardiac output
and myocardial perfusion.
 The IABP consists of a balloon which is connected to a
long catheter.
 The catheter is inserted via the femoral artery and
positioned such that the balloon sits in the descending
thoracic aorta.
 The balloon is also connected to a pump that allows it
to be inflated and deflated at designated intervals.
 IABP is indicated in
 selected cases of cardiogenic shock.
 cardiac failure after CABG and as a
 bridge to intervention for patients with acute
coronary syndromes, mitral regurgitation or
septal defects.

13. Extracorporeal membrane
oxygenation (ECMO)
 is a technique of providing a
temporary external circulation to a
patient with severe, reversible
cardiopulmonary failure.
 Blood is removed from the body via a
special cannula, pumped through the
ECMO circuit where it is oxygenated
in an oxygenator, and then returned
back to the body.
 ECMO use in the adult ICUis
exceedingly rare, but it is being
studied internationally.

14. Oxygen delivery
Oxygen delivery (DO2) Oxygen consumption (VO2)
 Is defined as the amount of gaseous
oxygen delivered to the body per
minute.
 It is determined by the cardiac
output and oxygen content of the
arterial blood (CaO2).
 DO2 = CO × CaO2
 CaO2 = (SaO2 × Hb × 1.34) +
(PaO2)(0.0031)
 Is the volume of gaseous oxygen
consumed by the body per minute.
 Oxygen consumption= Oxygen delivered
− Oxygen returned to the heart in venous
blood.
 It is a calculated value that is obtained by
knowing
 VO2 = [CO × CaO2] − [CO × CvO2]
 VO2 = (CO)(CaO2 − CvO2) × 10 dl/l

15. Shock
 Circulatory failure resulting in inadequate tissue
perfusion with consequent end organ/cellular hypoxia.

16. Classification of Shock

18. Treatment
 Treatment of shock begins with the
Airway, Breathing, and Circulation
model of treating any critically ill or
injured patient
 Treatment of the underlying cause
 Improving circulation and perfusion
is the cornerstone of shock
treatment
 Vasoactive drugs should not
routinely be part of initial
resuscitation efforts
 Patients may have several
aetiologies for their haemodynamic
compromise
 Frequently re-assessing responses to
therapy will ensure the best outcome

19. General Goals for Support of Shock Patients

20. Ventilation failure
 Hypoxaemic respiratory failure
(type 1)
 PaO2 ˂ 8 kPa (60 mmHg)
 Hypercapnic respiratory failure
(type 2)
 PaCO ˃ 6.7 kPa (50 mmHg)
Respiratory failure :
Oxygenation failure

21. Indications for Mechanical
Ventilation (MV)
 PaO2 ˂ 8 kPa (60 mmHg)
 PaCO2 ˃ 8 kPa (60 mmHg)
 Apnea or hypoventilation
 Rapid shallow breathing
 RR ˃ 35 bpm +Vt ˂ 5ml/kg
 Elective ventilation peri-operatively in high-
risk surgical cases
 Airway protection
 Airway obstruction
 (trauma/oedema/burn)
 Loss of ability to protect airway due to
neurological event (CVA/head injury)

22. Indications for
Tracheostomy:
 Prolonged ventilatory
insufficiency (2 weeks) may
be secondary to:
 Multiple chest injuries or
ARDS,
 long-term coma, or
 paralysis (spinal cord injury)
 Airway obstruction e.g.:
 maxillofacial trauma,
 pharyngeal oedema
 Post-laryngectomy/pharyngo-
laryngectomy

23. Types of MV
Volume support ventilation Pressure support ventilation
 A preset tidal volume is delivered
according to the rate that is set.
 A preset targeted peak airway and a
peak alveolar pressure.

24. Modes of MV
 A/C (volume/pressure):
 All breaths by ventilator
 Set Vt,RR,FiO2,PEEP,Peak flow
 SIMV (volume/pressure):
 Patient breaths+vent breaths
 Set Vt,RR,FiO2,PEEP,peak flow
 CPAP:
 Spontaneous breathing
 Set IPP,PEEP

25. O2-Haemoglobin dissociation
curveLung volumes
Ventilator Settings

26. Rapid Interpretation of Acid Base Abnormalities

27. Basic settings: Special settings:
 Mode of ventilation
(AC/SIMV/CPAP)
 Type of ventilation
(volume/pressure)
 FiO2 = 40 %
 Vt= 5-10 ml/kg
 RR= 10-14 bpm
 PEEP= 5 cmH2O
 Peek flow = 60 l/min
 Peak pressure ≤ 35 cmH2O
 I:E ratio = 1:2

28. Assessment
Oxygenation Ventilation
 PaO2
 Oxygen saturation
 PaCO2
 Capnography

29. Low PaO2 : High PaO2 :
 Increase FiO2
 Review Vt and RR
 Increase PEEP (may raise peak
airway pressure or reduce CO)
 Increase I:E ratio
 Increase pressure support/pressure
control
 CMV, increase sedation ± muscle
relaxants
 Consider tolerating low level
(‘permissive hypoxaemia’)
 Prone ventilation, inhaled nitric
oxide
 Decrease level of pressure
control/pressure support if Vt
adequate
 Decrease PEEP
 Decrease FiO2
 Decrease I:E ratio

30. High PaCO2 : Low PaCO2 :
 Increase VT (if low and peak airway
pressure allows)
 Increase RR
 Reduce rate if too high (to reduce
intrinsic PEEP)
 Reduce dead space
 CMV, increase sedation ± muscle
relaxants
 Consider tolerating high level
(‘permissive hypercapnia’)
 Decrease RR
 Decrease VT

31. Complications of Mechanical
Ventilation
 Ventilator-induced lung injury
 Ventilator associated pneumonia
(VAP)
 Haemodynamic instability
 positive pressure increases intrathoracic
pressure and can impede venous return to
the heart
 Technical complications
 Tube dislodgement,
 Kinking,
 Disconnections

32. Weaning from MV
 Reversal for the underlying cause of
respiratory failure
 Adequate oxygenation
 PaO2/FiO2 ratio ˃ 27
 PEEP ˂ 5–8 cmH2O
 FiO2 ≤ 40–50%
 Adequate ventilation and correction
of acid-base status PH ˃ 7.25
 Haemodynamic stability
 Capability to initiate an inspiratory
effort
 Capability to clear secretions.

33. Factors associated with
weaning failure:
 Increased oxygen cost of breathing
 Muscle fatigue
 hypophosphataemia, hypomagnesaemia,
hypokalaemia, malnutri tion, peripheral
neuropathy.
 Myopathy and drugs:
 muscle relaxants, aminoglycosides
 Inadequate respiratory drive
 alkalosis, opiates, sedatives, malnutrition,
CVA, coma.
 Inadequate cardiac reserve and heart
failure

34. Acute Lung Injury (ALI) Acute Respiratory Distress
Syndrome (ARDS)
 Acute onset of respiratory failure
 Bilateral chest infiltrates on frontal
radiograph
 Absence of elevated left heart filling
pressure (PAOP < 18 mm Hg)
 PaO2/FIO2 < 40 (300 mmHg)
 Acute onset of respiratory failure
 Bilateral chest infiltrates on frontal
radiograph
 Absence of elevated left heart filling
pressure (PAOP < 18 mm Hg)
 PaO2/FIO2 < 27 (200 mmHg)

35. Systemic inflammatory
response syndrome (SIRS): Sepsis:
 Two or more of the following:
 Temperature ˃ 38◦ or ˂36◦
 Tachycardia HR ˃ 90
 Tachypnoea :
 RR ˃ 20 or
 PaCO2 ˂ 4.3 kPa(32 mmHg)
 WBC :
 ˃ 12 000 or ˂ 4000 or
 ˃ 10% immature (band) cells
 SIRS + established focus of infection

36. Severe sepsis
 Sepsis + associated organ
dysfunction and hypoperfusion
as evidenced by one of the
following:
 Acute mental status change
 Systolic blood pressure :
 90 mmHg or
 decreased normal systolic pressure by ˃ 40
mmHg
 Lactic acidosis
 Hypoxaemia
 Oliguria
 Hyperbilirubinaemia
 Coagulopathy

37. Septic shock
 Severe sepsis + Hypotension
 Not responsive to
intravenous fluid
resuscitation or
 Need for inotropes or
vasopressors to maintain
blood pressure.

38. Acute Renal Failure (ARF)
 Increase in serum creatinine by
20–50% over baseline.
 Creatinine clearance ˂ 50%
 The need for renal replacement
therapy (RRT)
 Oliguria
 Urine output ˂ 400ml/day
 Urine output ˂ 0.5ml/kg/hr
 Anuria
 Urine output ˂ 50ml/day

39. Causes of ARF:
 Pre-renal
 Renal (ATN)
 Post-renal(obstructive)
 Vast majority of ARF (particularly in
surgical patients) is secondary to
renal hypoperfusion,
 The next important step is
determining whether the patient has:
 Pre-renal failure or
 ATN

41. Treatment
The two mainstays of therapy
in ARF :
 Appropriate volume expansion
 (Optimizing tissue perfusion without
pushing the patient into fluid
overload)
 Avoidance of any further nephrotoxic
insults.

42. Dopamine ? Loop diuretics ?
 A multitude of studies have
consistently found that
 dopamine does not prevent ARF in at-risk
patients,
 dopamine does not change the outcome in
patients with ARF.
 Studies have also failed to find
diuretics beneficial in either the
prevention or treatment of ARF.

43. Renal Replacement
Therapy(RRT)
 Indications:
 Acidosis
 Hyperkalaemia
 Fluid overload
 Severe uraemia
 Forms :
 Hemofiltration
 Hemodialysis

44.  The Standard method:
 CVVH
 Others:
 CVVHD
 IHD
 ? CAVH (complication)
 ? PD (not used in ICU)

45. Hemodailysis Hemofiltration
 Based on concentration gradient.
 blood is pumped through a
semipermeable filter. Electrolytes and
fluid move down a concentration
gradient into the dialysate fluid and it
is removed.
 Rapid blood flow rates over a 2–4 hour
duration
 Performed on a daily or every other
day basis.
 Associated with haemodynamic
instability and large fluid shifts.
 Based on pressure gradient
 blood is pumped through highly
permeable filter with hydrostatic
pressure driving ‘ultrafiltrate’ to be
collected.
 Replacement fluid and electrolytes are
added back to the concentrated blood
before its return to the body
 The blood flow is approximately 200
ml/hour
 It is a continuous 24-hour process

46. Continuous Veno-Venous Haemofiltration (CVVH)

47. Acute liver failure
The Aetiologies : Is the sudden development of liver
parenchymal injury resulting in
coagulopathy (INR ˃ 1.5) in a patient
who lacks underlying chronic liver
disease.
 Shock/ischemia
 MODS
 Viruses:
 hepatitis viruses A, B, C, D
and E, rarely herpes simplex,
varicella-zoster and CMV
 Drugs/toxins:
 paracetamol, isoniazid,
phenytoin, halothane, carbon
tetrachloride,
mushrooms(Amanita spp)

48. Hepatic encephalopathy
 In cirrhotic & chronic hepatic failure
encephalopathy is related to increased
ammonia levels.
 In FHF it is related to cerebral oedema.
 Worsening of encephalopathy is a sign of
progressive cerebral oedema and
 poor prognostic indicator.
 Grade 1: awake, mild confusion, altered
personality
 Grade 2: awake, agitated, disoriented,
hallucinations
 Grade 3: stuporous, but may be aroused
 Grade 4: comatose, but with intact
pupillary reflexes and usually ability to
withdraw to pain

49. Management
 The cornerstone of management is
treating the source of failure (if
possible) and systemic support.
 Liver transplantation
 is indicated in patients with FHF
and grade 3 or 4 encephalopathy
 Extracorporeal liver assist device
(ELAD) are still being developed and
evaluated.

50. Nutrition in ICU
Enteral nutrition Parenteral (TPN)
 NGT
 NDT/NJT
 Gastrostomy tube
 Jejunostomy tube
 Central venous
 Peripheral venous

51. Complication of TPN
 Fluid excess
 Hyperosmolar hyperglycaemic state
 Electrolyte imbalance
 Hypophosphataemia
 Metabolic acidosis Hyperchloraemia
 Rebound hypoglycaemia
 High endogenous insulin levels
 Vitamin deficiency
 Folate
 Thiamine
 Vitamin K
 Pancytopenia
 Encephalopathy
 Hypoprothrombinaemia
 Vitamin excess
 Vitamin A
 Vitamin D
 Dermatitis
 Hypercalcaemia
 Fatty l iver

52. Anti-Ulcer medication
 Risk of stress ulceration is increased
in the presence of:
 Sepsis
 Head injury
 Major surgical procedures
 Multiple trauma
 Severe burn injuries
 Respiratory failure
 Severe hepatic failure
 Severe renal failure
 Routine use of anti-ulcer drugs is
unnecessary.
 Use should be restricted to those
who have the risk factors & stopped
when patients are established on
enteral feeding.
 Patients who have a coagulopathy or
on NSAIDs, SSRIs, clopidogrel or
steroids (whether or not enterally
fed) should be covered with PPI or
ranitidine.
 The long term use of PPIs in the ICU
is associated with Clostridium
difficile infection.

53. Discharge from ICU
Patient improves Irreversibly deteriorates
 Stabilize,
 No longer require respiratory
support,
 Underlying illness corrected.
 Patient not improving and organ
support is only deferring death or
 if the patient enters a persistent
vegetative state or
 if the patient or the family wish to
pursue palliative care

54. Sometimes discharge from intensive care will mean a step down in the level of care
 Transfer to a high-dependency unit.
 Transfer directly to ward care