General Medical Principles

 Electrolyte Replacement
o 10 mEq K+ (oral or IV) raises plasma K+ by 0.1

 Insulin Requirements
o A unit of insulin is equivalent regardless of the formulation.

o Formulations
 Lispro/Aspart have a peak onset of 90 minutes and a duration of 3-4 hours
 Lantus has a duration of 24 hours
 Levemir has a duration of 12 hours

o Type 1 DM
 0.1 – 0.2 units/kg/24 hours
 So a 70 kg male will require 7-14 units per day

 Give 50% of insulin requirement as Lantus and 50% as Lispro

 When giving steroids, give NPH insulin (intermediate acting)

 0.05 units/kg/24 hours per 10 mg prednisone
 Max dose of 0.2 units/kg

o Type 2 DM
 If on oral hypoglycemics
 0.3 – 0.5 units/kg/24 hours (higher dose due to resistance)

 If on home insulin, look at their home insulin dose and use that to calculate their 24 hour insulin
requirement. Remember that a unit of insulin is equivalent regardless of the formulation.

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 Ventilators
o Typical ventilator settings
 VT of 500 mL, frequency of 12 breaths/min, FiO 2 100%, PEEP 5 cm H2O

o General Principles
 Ventilated and bleeding patients should always be on a PPI.
 Vigileo monitor is used in intubated patients with rapid boluses of IVF to determine if
hypotension is volume responsive.

o Acute Respiratory Distress Syndrome (ARDS)

 Defined as hypoxemia with bilateral infiltrates of non-cardiac origin
 PaO2/FiO2 ratio (PF ratio) is the ratio of arterial O 2 partial pressure to fractional inspired O2
 PF ratio > 300 is normal, decreasing values indicate increasing levels of hypoxemia

 PF ratio < 100 indicates ARDS

 o Hypercapneic Respiratory Failure
 Minute ventilation = respiratory rate x tidal volume
 CO2 levels are affected by minute ventilation.
 It can be dangerous to drive off CO2 by increasing the RR, especially in patients with
underlying COPD, because it can lead to air trapping (auto PEEP)
 It is best to first increase VT as this recruits more alveoli. Monitor for barotrauma by
measuring the plateau pressures. Aim for pressures < 30 cm H 2O

o Evaluation criteria for extubation

 PF ratio > 150
 SpO2 > 90% with FiO2 < 40% and PEEP < 5
 Hemodynamic stability
 Inspiratory effort
 Rapid shallow breathing index (RSBI) = RR/V T must be < 100. The lower the better.

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 Acute Renal Failure

o General Principles
 Urine specific gravity
 Normal 1.010
 Dry 1.030
 Wet 1.000

 Pre-renal
 FENa < 1%
 FEUrea < 35% (if on diuretics)

o Acute Tubular Necrosis (ATN)

 Pathology of the renal tubules
 60% of all cases of ARF
 Muddy brown casts are pathognomonic
 Causes: contrast, bouts of hypotension, antibiotics, protein
 Treated by hydration and cessation of offending agent

o Acute Interstitial Nephritis (AIN)

 Pathology of the interstitium surrounding the renal tubules.
 Typically caused by adverse drug reactions – NSAIDs, sulfa drugs, antibiotics
 Treated by removing the offending drug. Steroids do not clearly help
 Characterized by sterile pyuria and/or eosinophiluria

o Glomerular pathology
 Characterized by proteinuria. Evaluate using Protein:Cr ratio
 Red cell casts indicate nephritic syndrome.

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  Systemic Approach to EKG
o Identify rhythm
o If QRS > 0.12 check V1 and V6 for BBB
 RBBB
 Wide QRS > 0.12 sec in V1
 T wave inversion in V1
 rSR’ or RR’ configuration
 Mostly positive complex in V1

 LBBB
 Wide QRS > 0.12 sec in V6
 T wave inversion in I, AVL, V6
 Negative complex in V1

o Examine consecutive leads for ischemia/infarction

 Ischemia
 T-wave inversion and/or ST depression
 Note: T-wave inversions in inferior leads are not pathological

 Infarction
 Acute (minutes to hours): ST elevation, tall T waves
 Evolving (hours to days): Deep T waves, Q waves (only significant if > 0.04 sec or if the
depth > ¼ size of the R wave
 Note: Q waves in V1 are not pathological

o Check for atrial hypertrophy

 RAH (P Pulmonale) – tall, narrow P wave in II, III, AVF
 LAH (P Mitrale) – Wide, humped, or biphasic P wave in V1

o Determine axis

o Check for ventricular hypertrophy

 RVH – tall R waves in right chest leads, right axis deviation, T wave inversion in V1-V3
 LVH – S wave in V1 + R wave in V5 or V6 > 35 mm, R wave in AVL > 13 mm, T wave inversion in
AVL, I, V5, V6.

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 Sepsis and Septic Shock

o Pneumonia is the most common cause (50% of cases) followed by intra-abdominal infections and UTIs.

o Early Goal Directed Therapy

 Maintain CVP between 8-12 with IV fluids
 Maintain MAP between 65-90 with vasopressors
 Maintain SvO2 > 70 by keeping Hct > 30 and maintaining cardiac output with dobutamine
 Resuscitation Fluids
o Colloid solutions do not offer substantive hemodynamic advantages over crystalloid solutions.
o The use of albumin is associated with increased mortality among patients with TBI due to increased ICP.
o Normal saline has been associated with the development of hyperchloremic metabolic acidosis and AKI.
The cause is due to volume expansion and bicarbonate dilution leading to renal bicarbonate wasting.
o The safety of hypertonic solutions has not been established, specifically in patients with TBI.

 Traumatic Intracranial Hypertension

o Normal ICP in adults is below 15 mm Hg. Anything above 20 mm Hg is pathologic and should be treated.
o Mass lesions causing herniation
 Falcine herniation – a hemisphere is displaced medially
 Uncal herniation – a monolateral pressure gradient pushes
the medial edge of the temporal lobe (uncus) through the
tentorial foramen.
 The third cranial nerve and the posterior cerebral
artery are compressed, causing unilateral pupillary
dilation, a lack of reactivity to light, and infarction.
 The brain stem is distorted and compressed, with
early impairment of consciousness.
 Central herniation – a bilateral, homogeneous increase in
ICP in the supratentorial space displaces the brain
downward through the tentorial foramen.
 The brain stem is compressed and displaced downward without signs of lateralization
and with bilateral pupillary abnormalities.

o Vascular effects of ↑ICP are caused by impaired cerebral perfusion pressure which is the driving force
for cerebral blood flow
 CPP = MAP – ICP
 As the CPP ↓, CBF may become insufficient for adequate brain-tissue perfusion. Ischemia will
induce further cytotoxic edema and result in even ↑ICP

o Medical Therapy
 Mannitol or hypertonic saline
 Reduce the cerebral blood volume by extracting water from the brain across the BBB.
 The effect only lasts for several hours until the osmotic equilibrium is reestablished.
 The integrity of the blood-brain barrier is a prerequisite for use.

 Hyperventilation
 Reduces ICP at the expense of decreasing CBF as a result of vasoconstriction.
 Carries a risk of cerebral ischemia. Guidelines recommend monitoring oxygen saturation
in the jugular bulb and monitoring of brain-tissue oxygenation.

 Barbiturates
 Depress cerebral metabolism and reduce CBF, causing a decrease in cerebral blood
volume and therefore ICP.
 Carry a risk of cardiac depression and arterial hypotension.
 Cardiac and Pulmonary Physiology
o The idea behind transfusing blood is to increase oxygen delivery to tissues.
o When inadequate oxygen is delivered, cells switch to anaerobic metabolism and begin producing
lactate. Cells begin producing lactate at 50% oxygen extraction.
o Every liter of supplemental oxygen adds ~3% to the FiO 2

o Alveolar gas equation

 PAO2 = 713 (FiO2) – 1.25 (PaCO2)
 Hypercapnia (hypoventilation) thus decreases oxygenation. Increasing the FiO 2
compensates for this. As little as 30% FiO2 can negate the effects of hypoventilation.

 Alveolar gas equation at room air

 PAO2 = 150 – 1.25(PaCO2)

o Arterial oxygen content

 CaO2 = (SaO2 )(Hb)(1.34) + 0.003(PaO2)

o Oxygen extraction
 Oxygen uptake into cells must remain constant to meet a cell’s oxygen consumption needs.
Normal O2 consumption = 250 mL/min.
 O2 uptake = O2 delivery x O2 extraction
 Oxygen delivery = CO x CaO2
 The body tries to maintain a constant O 2 delivery to tissues. If CaO2 falls, the body compensates
by increasing cardiac output.
 If O2 delivery to cells does not meet metabolic demand, O 2 extraction will increase. The
maximum O2 extraction is about 50%. Therefore, an O2 extraction of 50% could be used as a
trigger point for transfusion.
 O2 extraction is roughly equivalent to SaO 2 – ScvO2.