![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](https://image.slidesharecdn.com/fundamentalsoficu-151005192726-lva1-app6891/85/Fundamentals-of-ICU-14-320.jpg)
Fundamentals of ICU
- 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.
- 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
- 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