Categories of ICU Patients
Preoperaive. Patients needs intensive care and monitoring, for possible interventions: CAD patient going for PCI or heart surgery. Head trauma, stroke patient going for neurosurgery. Multitrauma patient going for general, orthopedic, and other surgeries.
Post-operative recovery.
Bruns care.
Neurosurgical critical care.
MICU. hemodynamic insufficiency, respiratory failure, sepsis, toxic ingestions, DKA, fluid and electrolyte abnormalities, deteriorating level of consciousness, and coma.
Standard Stress Response
Stress response - acute compensation, followed by hypermetabolism and catabolism and, after 4 to 7 days, resolution with fluid mobilization and anabolism.
Death in ICU
Most patients die due to withdrawal of life support. They die because their multi-organ dysfunction, loss of physiologic reserve and neuroendocrine exhaustion is irreversible.
Creatinine Clearance
For measuring renal reserve in an ICU patient, the most efficient way of quantifying is through measurement of 24 hour creatinine clearance. Serum creatinine is a poor measure of renal function.
MODS
“Multi-Organ Dysfunction Syndrome” is the internationally recognized term to describe loss of physiologic reserve and progressive organ injury through failure associated with critical illness.
Critical Care Scoring Systems
Apache I, II & III, SAPS, MPM, MOF score and SOFA, MODS
Shock
Shock is acute circulatory failure leading to inadequate tissue perfusion and end organ injury
Cardiogenic. Malfunction of the pump (cardiogenic)
Ischemia, MI, PE, arrhythmias, CHF
Distributive. Malfunction of the tubing
Sepsis, anaphylaxis, neurogenic
Hypovolemic. Problem with the fluid.
Hemorrhage, burns, fluid losses, pancreatitis, cirrhosis, CHF, nephrotic syndorme (third spacing)
Sepsis
Systemic inflammatory response syndrome (SIRS) is tachycardia, tachypnea, pyrexia (or hypothermia), leucocytosis or leucopenia, all without identification of an infective organism .
Sepsis is SIRS with source - an organism is identified
Severe sepsis is sepsis with hypotension or hypoperfusion.
Septic shock. severe sepsis and refractory hypotension, despite pressors.
Presenting patient In ICU rounds
This is Mr John Doe, he is 74 years old, day 7 in ICU post repair of a ruptured abdominal aortic aneurysm. He has a background history of coronary arterial disease, three vessel CABG in 1997 and hypertension well controlled with lisinopril.
His post operative course has been complicated by early respiratory insufficiency, a non-ST segment elevation myocardial infarct, massive blood transfusion and acute renal failure requiring continuous dialysis, now discontinued.
His main current problem is failure to wean from mechanical ventilation; a tracheostomy is planned. Other problems include polyuric renal failure, hypokalemia, hyperbilirubinemia, a grade 2 decubitus ulcer on his sacrum and dehiscence of his abdominal wound.
Neurological
The patient responds to verbal stimuli, his GCS is 11, his Ramsay score is 3 on propofol 10mg/minute, and fentanyl 25mg/hour.”
Respiratory
Patient’s blood gas on an FiO2 of 0.4 and PEEP of 10cmH2O is pH 7.38, PaCO2 44, PaO2 77, HCO3 27, Saturation 95%, written as ABG on 40% and PEEP: 10 is 7.38/44/77/27/95%. His ventilator settings AC-12, Vt: 500, FiO2: 0.7, PEEP: 5, written as AC-12/500/70/5. His chest x-ray reveals low lung volumes, bilateral infiltrates and small bilateral pleural effusions. He requires hourly suctioning and his sputum is thick and purulent.
Cardiovascular
Pulse rate is 100, in atrial fibrillation, on amiodarone, his blood pressure is 90/50 on dopamine 5mg/kg/minute, his CVP is 12, following volume loading of 5 litres, our target BP is MAP of 60 and CVP of 14cmH20. He has a PA catheter in situ: is PAP is 38/18, wedge pressure of 14cmH20, which correlates well with the CVP, his cardiac output is 8.0 litres and his cardiac index is 2.6 litres, again on dopamine. His SvO2 is 71%, up from 53% on admission.
Gastrointenstinal
On examination of the abdomen, there is a midline laparotomy wound, which is healing well. Nasogastric suction is minimal. He is being fed thru a post-pyeloric feeding tube, using enteral feed at 80ml/hour, which is his goa (the feed is contains…)l. The feed is well tolerated and he is passing stool. His liver function has been normal since admission
Renal/Fluid balance
Patient is 8 litres positive since admission, 500ml positive over the last 24 hours. His urinary output is on average 35ml/hour. His urea is 20 and his creatinine is 1.8, up from 1.4 over the past 24 hours. We have sent a urinary sodium and creatinine in order to determine the nature of the renal injury
ID
The patients temperature is 38.6, his white cell count is 19. He has an infiltrate on the right lower zone of his chest x-ray. A broncho-alveolar lavage was performed 2 days ago, and Pseudomonas grew. He is being treated with ciprofloxacin (dose) and gentamycin (dose). He has a penicillin allergy, and is on day 3 of 10 of treatment. We have also sent blood, urine and stool cultures
Hematology
His hemoglobin is 9.2 following transfusion of 4 units of red cells. His platelet count is 230 and his prothrombin time (to control) ratio is 1.2 (the INR is used only to guide warfarin treatment.
Endocrine
Patient’s blood sugar is 240mg/dl, controlled on an insulin drip, currently at 5 units per hour. He is being treated with hydrocortisone at 50mg q8hours, due to chronic steroid use, related to COPD.” Alternatively, “he is being treated with hydrocortisone 50mgq8hours due to adrenal insufficiency related diagnosed by a positive ACTH stimulation test
Integumentary/Extremities
On examination of the skin and extremities, the patient has a stage 2 decubitus ulcer on his sacrum. There is some peripheral edema and the patient is being treated with sequential compression devices and enoxparin for DVT prophylaxis. The laparotomy wound site is clean and granulating
Analgesia
The patient’s pain score is 2/10 and he is being treated with a hydromorphone/bupivicaine epidural (at protocoled concentrations) at 4ml/per hour. In addition he is receiving acetaminophen 1gq6hours, and ketorolac 15mg iv q8hours. This will be discontinued tomorrow
Devices/lines/drains
The patient has a right radial arterial line, which is 6 days old, a right sided subclavian line, which is 4 days old, and two abdominal drains, which drained 300ml and 200ml of sero-sanguinous fluid over the past 24hours. All of the sites look clean
Lab
Radiology
Medications
GI/DVT Propylaxis
Code Status
ICU note
9/9/02 8.15am
Mr John Doe age 74y
Day 8 post AAA, complicated by 1. Resp Failure 2, ARF (CVVHD) 3. NSTEMI 4. Massive transfusion
Background: CABG x3 (1997), HTN (lisinopril)
Current Problems
1, Failure to wean
2. Polyuric renal failure
3. Coronary ischemia
4. Hyokalemia
5. Increased bilirubin
6. Saccral Decubitus
7. Wound dehiscence
ROS
Neuro – Ramsay 4 on midazolam 4mg/hr, morphine 2mg/hr.
Resp – FiO2 40%, PaO2 78 on PC 20 PEEP 5, rate 12. Not weaning. ABG 7.46/78/48/+2/94%, Crackles audible throughout, dull in bases. CXR – bilateral infiltrates (ARDS)
CVS – BP 120/70, HR 92 (metoprolol 5mgq6h), CVP 8, normal HS, No murmurs, ECG T-wave iversion across anterior leads.
GI – abdomen soft, non tender, wound open but clean, post-pyeloric feed started (30ml/hr), no stool, Bilirubin has increased to 12.6, transaminases are normal.
Renal – balance -500ml (x24h), overall +ve 8l. Creatinine 2.4 (down from 2.6). Hourly outpur 80-120ml.
Endocrine – no problems
Extremities – mild ankle edema, SCDs, enoxaparin 30mgq12, large (6 x 6cm) grade 2 pressure sore over sacrum
Labs - 138/3.2/111/29 Hb 9.0 (1 unit RCC overnight), plat 230, PTR 1.5
ID - Temp 38.2, WCC 19.2, pseudomonas in BAL x 2/7, tx cipro 200 bid, gent 350mg qd
Devices – RSCL, RRAL
Impression
ALI not resolving – infectious component, no current role for steroids. Heart rate remains a little fast in setting of ischemia – cardiology should review with regard to possible PCI. High bilirubin may be due to hemolysis (massive transfusion), cholestasis or sepsis. Renal function is returning, although K+ spillage requires vigorous supplementation (required for muscle function). Wound is healing well. Decubitus appears to be enlarging.
Plan
Neuro – DC midazolam today and assess neurologically
Resp – Trach tomorrow
CVS – increase metoprolol to 10mg q6h, cardiology to see ?PCI
GI – increase feeds to goal 75ml/h, administer PO4 enema
Renal – replace K+ losses with KPO4
Endocrine – NAD
Extremeties – wound care to see decubitus
Heme/labs – transfuse if Hb < 9, hx of CAD – continue ASA
ID – continue antibiotics x 5/7
Devices – remove central line, use peripheral veins pro temps
Cardiac Output: The forces that govern cardiac output are:
Preload: The load imposed on the resting muscle that stretches the muscle to a new length, measured as end-diastolic pressure/end diastolic volume.
End-diastolic pressure is an accurate reflection of preload only when ventricular compliance is normal. Changes in EDP accurately reflect changes in preload only when the ventricular compliance is constant.
End-diastolic volume of the ventricles is the preload force of the intact heart.
According to the length-tension relationship of muscle, an increase in the length of a resting (unstimulated) muscle will increase the force of contraction when the muscle is stimulated to contract. Therefore, the preload force augment the force of muscle contraction.
Afterload: The total load that must be overcome or moved by a muscle when it contracts, measured by systemic and pulmonary vascular resistances.
The forces that contribute to ventricular afterload can be identified using the components of the Laplace relationship. There are three major contributing forces: pleural pressure, arterial impedance, and end-diastolic volume (preload). Preload is a component of afterload because it is a volume that must be moved by the ventricle during systole.
The principal determinant of ventricular afterload is a hydraulic force known as impedance that opposes changes in pressure and flow. Aortic impedance is the major afterload force for the left ventricle and pulmonary impedance serves the same role for the right ventricle. Impedance is influenced by two other forces:
Force that opposes the rate change in flow, known a compliance
Compliance is the distensibility of the ventricle = change in end-diastolic volume by end diastolic pressure. ∆EDV/∆EDP
Force that opposes steady flow, called resistance. Resistance is a force that opposes nonpulsatile flow.
Contractility: The velocity of muscle contraction when muscle load is fixed.
Frank-Starling relationship of the heart: In the normal heart, diastolic volume is the principal force that governs the strength of ventricular contraction.
Ventricular function curves is used to monitor the relationship between preload and systolic performance. EDP is used as the clinical measure of preload because end-diastolic volume is not easily measured.
Law of Laplace states that the tension (T) in a thin-walled sphere is directly related to the chamber pressure (P) and radius (r) of the sphere: T = Pr. In the heart, T represents the peak systolic transmural wall tension of the ventricle, P represents the transmural pressure across the ventricle at the end of systole, and r represents the chamber radius at the end of diastole.
Positive pleural pressure can promote ventricular emptying by facilitating the inward movement of the ventricular wall during systole. This response indicates that positive intrathoracic pressure can provide cardiac support by "unloading" the left ventricle.
Negative pleural pressures surrounding the heart can impede ventricular emptying by opposing he inward displacement of the ventricular wall during systole. This effect is responsible for the transient decrease in systolic blood pressure (reflecting a decrease in cardiac stroke volume) that normally occurs during the inspiratory phase of spontaneous breathing. When the inspiratory drop in systolic pressure is greater than 15 mm Hg, the condition is called "pulsus paradoxus" - a misnomer, since the response is not paradoxical, but is an exaggeration of the normal response.
SVR = SAP - RAP/CO
PVR = PAP - LAP/CO
When Palv > LAP: PVR = PAP - Palv/CO
SAP is mean systemic arterial pressure.
RAP is mean right atrial pressure.
PAP is mean pulmonary artery pressure.
LAP is the mean left atrial pressure.
CO is cardiac output.
The SAP is measured by an arterial catheter, and the rest of the measurements are obtained with a pulmonary artery catheter.
Oxygen Transport Formulae:
Transport of O2 from lungs to tissues can be described by four clinical parameters:
Concentration of oxygen in blood
O2 content = 1.34 x Hb x SO2 (O2 saturation of Hb)
SO2 is derived from HbO2/total Hb
Delivery of oxygen in arterial blood
DO2 = CaO2 x Q (cardiac output) x 10
DO2 = Q x 1.34 x Hb x SaO2 x 10
Rate of oxygen uptake from capillary blood into the tissues
VO2 = Q x (CaO2 - CvO2) x 10
The equation above is a reverse Fick euation for Q (cardiac output)
Q = VO2/CaO2 - CvO2
VO2 = Q x 1.34 x Hb x (SaO2 - SvO2)
VO2 = Ve (minute vent) x (FiO2 - FeO2). FiO2
Does not include O2 consumption of the lungs which is normally <5%, of the whole body VO2, but can increase up to 20% in inflammatory conditions in the lungs, like pneumonia.
Elevated in exercise, postop, thyrotoxicosis.
Decreased in hypoxemia, lactic acidosis.
VO2 = DO2 x O2ER
DO2:VO2 rato of 4:1 or higher has been recommended as a management strategy to avoid he anaerobic threshold in critically ill patients.
Fraction of oxygen in capillary blood that is taken up into the tissues
O2ER = (SaO2 - SvO2)/SaO2
Increased in cardiogenic and hypovolemic shock
Decreased in Septic shock, sever liver disease and systemic A-V fistulae
Arterial O2 content (CaO2)
CaO2 = (1.34 x Hb x SaO2) + (.003 x PaO2) = 20 vol %
O2 content = 1.34 x Hb x SO2.
Venous O2 content (CvO2)
CvO2 = (1.34 x Hb x SvO2) + (0.003 + PvO2) = 15 vol %
Normal levels of O2 in Arterial and Venous Blood
PaO2 is used to assess he efficiency of gas exchange in the lungs, and not arterial oxygenation.
Normal ranges of O2 and CO2 Transport Parameters
Normal Levels of CO2 in Arterial and Venous Blood
The Haldane Effect:
Hb has a greater buffering capacity when it is in the desaturated form, and blood that is fully desaturated can bind an additional 60 mL/L of CO2. The increase in CO2 content that results from oxyhemoglobin desaturation is known as the Haldane effect. The CO2 content in venous blood is 40 mL/L higher than in arterial blood. 60% of the increased CO2 content in the venous blood is due to an increase in PCO2, while 40% is due to oxyhemoglobin desaturation. Thus the Haldane, effect is responsible for almost half of the rise in CO2 content in venous blood.
VCO2 = Q x (CvCO2 - CaCO2)
RQ = VCO2/VO2 = 0.8
The normal rate of acid excretion via the lungs is 9 mEq/min or 12,960 mEq in 24 hours. Since the kidneys excrete only 40 - 80 mEq of acid every 24 hours, the principal organ of acid excretion in the body is the lungs, not the kidney