I. Basic 4 Shock Electrolytes and Fluid

In adults - 7% of body weight 

In children - 8-9% of body weight

• Cardiogenic (Heart) -
• - Extrinsic abnormalities (such as tension pneumothorax,hemothorax, or tamponade)
• - Intrinsic abnormalities (such as pump failure due to infarct, cardiac failure, contusion, cardiaclaceration).

Hemorrhagic (Large vessels) -  Bleeding

Distributive (Small vessels) - neurogenic dysfunction or sepsis

• Class I - <15%, Anxiety only, vitals normal 
• Class II – 15-30% , Pulse >100
• Class III – 30-40%, Pulse >120, BP decreased, Output decreased
• Class IV - >40% , Pulse >140, BP decreased, output negligible

Hemodynamic signs less reliable in elderly patients and patients with beta-blockers.

Patients in shock do not always have the physiologic changes as taught in the ATLS course, and a high degree of variance exists among patients. 

Children seem to be able to compensate, even after large volumes of blood loss, because of the higher water composition of their bodies. However, when they decompensate, it can be rapid.

Older patients do not compensate well; when they start to collapse physiologically, the process can be devastating because their ability to recruit fluid is not as good and their cardiac reserves are less.

• RL – more physiological
• Packed RBC are preferred to whole blood.

Arterial - faster bleeding, rapid hypotension, ischemia has not yet occured - lactate is normal 

Venous - Slower bleeding, body has time to compensate, large blood volume is lost before hypotension develops, more time for ischemia - increase lactate.

• No of milimole of base required to correct the pH of liter volume of blood to 7.4 
• Normal value - -2 to +2  mEq/lit 
• Base excess >+3 - metabolic alkalosis 
• Base excess <-3 - metabolic acidosis 
• In renal failure patients, based deficit of >6mmol/lit is associated with poor outcome

• Metabolic acidosis - due to increased lactate due to anaerobic respiration 
• Hypothermia - no delivery of nutrients to tissues - no ATP - hypothermia 
• Coagulopathy- hypothermia and acidosis affects the efficacy of enzymes (that work best in 37 C) and optimal pH

[@ MCH]

• Bicarbonate 
• THAM (tromethamine; tris[hydroxymethyl] aminomethane)

Dose of bicarbonate required - (0.3X base defecit X weight) / 9

• Trauma - 
• Mild - 36-34 C 
• Moderate - 34-32 C 
• Severe - <32 C 

• Medical (Accidental) 
• Mild - 35-32 
• Moderate - 32-28 
• Severe - <28

• Normal basal metabolic rate heat generation - 70kCal/hr 
• Shivering - 250kCal/hr

Passive – Dry the patient, Warm fluids, warm blankets, Head covers, Warm the room

• Active
• External – Blair hugger, heated warmers, Lamps, radiant warmers
• Internal – Warmed fluids, heat ventilator, cavity lavage,  continuous arterial or venous rewarming, full or partial bypass

• - Airway from vent - 9
• - Overhead radiant warmers - 17
• - Heating blankets - 20
• - Convective warmers - 15-26
• - Body cavity lavages - 35
• - Continuous arteriovenous rewarming - 92-140

• Forced air heating increases only the patient’s ambient temperature, but it can actually cool the patient initially because it increases evaporative heat loss if the patient is wet from blood, fluids, clothes, or sweat.
• Warming the skin may feel good to the patient and the surgeon, but it actually decreases shivering (a highly efficient method of internal warming that tricks the thermoregulatory nerve input on the skin).
• Because forced-air heating uses convection, the actual amount of active warming is estimated to be only 10 kcal/hr

• PT and aPTT - the traditional tests are performed at normal pH and temperature, so they cannot take into account the effects of hypothermia and acidosis on coagulation. The traditional tests of coagulation are performed on serum and not on whole blood, so they are unable to measure the interaction of coagulation factors with platelets.
• Thromboelastography and rotational thromboelastometry - based on similar principles of
• detecting clot strength, which is the final product of the coagulation cascade. They are also performed on whole blood, so they take into account the functional interaction of coagulation factors and platelets.

• Recombinent factor VIIa (rFVIIa)
• Prothrombin complex concentrate
• Tranxemic acid (Antifibrinolytic)

• Permissive hypotension until definitive surgical control
• • Minimize crystalloid use
• • Initial use of 5% hypertonic saline
• • Early use of blood products (PRBCs, FFP, platelets, cryoprecipitates)
• • Consider drugs to treat coagulopathy (rFVIIa, prothrombin concentrate, TXA)

• 
• Plasma lyte and Normosol are more physiological than LR. LR is more physiological than NS. 
• RL contains calcium. When transfusion is required, LR has to be switched to NS, as LR contains calcium and it promotes coagulation.  
• Baxter (Plasma lyte) - also contains aetate, gluconate and magnesium 
• Plasma lyte has advantage that it contains magnesium that reduces the need of magnesium replacement. 
• From the chloride point of view, LR may be better than Plasma-Lyte, which may be better than normal saline. In a large volume, there may be advantages of resuscitating with LR as it has the least amount of chloride

• Dilution of serum bicarbonate (HCO3−) through the replacement of lost plasma with fluids that
• do not contain bicarbonate. Normally, chloride and bicarbonate ions are reciprocated up or down with each other. Often, the result of massive normal saline infusion is a hyperchloremic anion gap
• metabolic acidosis. At extreme levels, acidosis can impair cardiac performance and decrease responsiveness to cardiac inotropic drugs. Many would argue that for cellular protection, the human
• body offloads oxygen more easily from hemoglobin in the acidotic state and that acidosis, at least to a degree, is actually better for a patient than alkalosis.
• No evidence exists that hyperchloremic acidosis does anything more than confuse the interpretation of the metabolic state.

Total 60% of fluid, 40% is intracellular, 20% extracellular. Among 20% - 15% interstitial, 5% - plasma

For adults weighting >40kg, (40+weight in kg) – maintainence fluid in ml/hr. For eg, 73 kg gets 40+73 = 113ml/hr

• 2-3gm/day
• Molar mass of NaCl – 58.4gm/mole
• NS contains 154mmol or 0.154mole – 0.154X58.4 = 9gm of sodium chloride in 1 liter of NS

• Blood urea nitrogen to creatinine ratio
•  > 20 - dry side
• < 10 - wet side

Such generalizations are true only for patients with normal renal function.

• High outputgenerally will mean that the body is trying to rid itself of water;surgeons should assist it by decreasing the maintenance fluid rate.
• In older patients with heart failure or sepsis who are intravascularly hypovolemic, anasarca can be profound. Many such patients will need more IV fluids despite having anasarca. To help estimate vascular volume, central venous pressure and data from pulmonary artery catheters (if available) are useful.
• HR does not help, varies due to pain, anxiety or temperature 
• In a healthy patient who does not have pneumonia,sepsis, or pulmonary contusion, the P/F ratio can reflect interstitial or lung water status; it will help direct what the maintenance rate should be.

Normal sodium level - 135-145 mEq/L 

• Mild - 130-138 
• Moderate - 120-130 
• Severe - <120 

Sodium level is lowered by 1.6mEq/lit for every 100mg/dl of glucose above 100.

• 1. Hypovolemic 
• - Vomiting, Diarrhoea 
• - Renal sodium loss, 

• 2. Euvolemic (water retention )
• - Primary polydipsia 
• - Excess IV fluids with no sodium 

• 3. Hypervolemia 
• - Cardiac failure 
• - Renal failure 
• - Liver failure

• Mild-moderate - Asymptomatic 
• Severe - Headache, Lethargy, Seiure, Coma

• 1. Acute Hyponatremia (<48 hours)
• - Hypertonic saline (3%, 5%, 23%) via central catheter
• - Sodium concentration should not be raised by 0.5% mEq/hr (>12mEq/L/day)

• 2. Chronic hyponatremia (>48 hours)
• - Never use hypertonic saline 
• - Correct by salt infusion like NaCl 0.9% to correct the underlying cause 
• - If hypertonic saline is used - it may cause central pontine myelinolysis.

• Etiology 
• - ADH secreting tumors - carcinoid, small cell carcinoma of lung 
• - Encephalitis, TB meningitis 
• - Brain tumors 
• - Psychiatric disorders 

• Diagnosis 
• - Serum low sodium level 
• - Urine output low 
• - Urine sodium increased 
• - Urine osmolarity - increased 
• - Serum osmolarity - decreased 

• Treatment - 
• - Water restriction 
• - Demiclocycline

• Moderate - 146-159 
• Severe >160

• Hypovolemic - Diuretics 
• Euvolemic - DI 
• Hypervolemic - Administration of too much saline

• Pitting edema 
• Increased urination 
• Dilated jugular veins
• Features of pulmonary edema

Recommendations are as follows:

• Establish documented onset (acute, < 24 h; chronic, >24h)
• In acute hypernatremia, correct the serum sodium at an initial rate of 2-3 mEq/L/h (for 2-3 h) (maximum total, 12 mEq/L/d).
• Measure serum and urine electrolytes every 1-2 hours
• Perform serial neurologic examinations and decrease the rate of correction with improvement in symptoms
• Chronic hypernatremia with no or mild symptoms should be corrected at a rate not to exceed 0.5 mEq/L/h and a total of 8-10 mEq/d (eg, 160 mEq/L to 152 mEq/L in 24 h).
• If a volume deficit and hypernatremia are present, intravascular volume should be restored with isotonic sodium chloride prior to free-water administration.

• The TBW deficit in the hyperosmolar patient that needs to be replaced can be roughly estimated using the formula 
• TBW deficit = correction factor x premorbid weight x (1 - 140/Na+)

• Equation 1: TBW = weight (kg) x correction factor
• Correction factors are as follows:
• Children: 0.6
• Nonelderly men: 0.6
• Nonelderly women: 0.5
• Elderly men: 0.5
• Elderly women: 0.45

• Equation 2: Change in serum Na+ = (infusate Na+ - serum Na+) ÷ (TBW + 1)
• Equation 3: Change in serum Na+ = ([infusate Na+ + infusate K+] – serum Na+) ÷ (TBW + 1)
• Equation 2 allows for the estimation of 1 L of any infusate on serum Na+ concentration. Equation 3 allows for the estimation of 1 L of any infusate containing Na+ and K+ on serum Na+.
• Common infusates and their Na+ contents include the following:
• 5% dextrose in water (D 5 W): 0 mmol/L
• 0.2% sodium chloride in 5% dextrose in water (D 5 2NS): 34 mmol/L
• 0.45% sodium chloride in water (0.45NS): 77 mmol/L
• Ringer's lactate solution: 130 mmol/L
• 0.9% sodium chloride in water (0.9NS): 154 mmol/L

•  An obtunded 80-year-old man is brought to the emergency room with dry mucous membranes, fever, tachypnea, and a blood pressure of 134/75 mm Hg. His serum sodium concentration is 165 mmol/L. He weighs 70 kg. This man is found to have hypernatremia due to insensible water loss.
• The man's TBW is calculated by the following:
• (0.5 x 70) = 35 L
• To reduce the man's serum sodium, D5 W will be used. Thus, the retention of 1 L of D5 W will reduce his serum sodium by (0 - 165) ÷ (35 + 1) = -4.6 mmol. The goal is to reduce his serum sodium by no more than 10 mmol/L in a 24-hour period. Thus, (10 ÷ 4.6) = 2.17 L of solution is required. About 1-1.5 L will be added for obligatory water loss to make a total of up to 3.67 L of D5 W over 24 hours, or 153 cc/h.

Serum potassium level <3.5 mEq/L

• Causes of hypokalemia 
• - Renal loss - diuretics 
• - Extra-renal loss - vomiting, NG tube, Diarrhoea, high output enteric or pancreatic fistula, CCF, 
• - Insulin therapy 
• - Beta-agonist 

• Clinical features of hypokalemia 
• - fatigue 
• - weakness 
• - ileus 
• - Flaccid paralysis 
• - Nephrogenic DI due to long standing hypokalemia 

ECG - Flat T-wave, U wave, ST depression 

• Management - 
• - Treatment of cause 
• - Potassium supplementation 
• a. Orally
• b. IV - if cardiac, neuromuscular complains present, or if potassium level < 2.5 mEq/L

• Concentration of administration of potassium 
• - 40 mmol/100ml via central line 
• - 10 mmol/100ml via peripheral line 
• - Serum potassium increased by 1mEq/L for every 100 mEq of potassium. 

• Rate of infusion 
• - Central line - 20 mmol/hr (maximum upto 40 mmol/hr) under cardiac monitoring
• - Peripheral line - 10 mmol/hr

Potassium level > 5.0 mEq/L 

• Causes 
• - Renal failure 
• - Cellular injury - sepsis, rhabdomyolysis, impaired aldosterone function 
• - Potassium sparing diuretics - Amiloride, Triamterene, spironolactone
• - Drugs - triamterone, beta blockers, succinylcholine

• Clinical features 
• - Asymptomatic 
• - Cardiac arrythhmia 
• - Cardiac arrest 

• ECG 
• - Tall T wave 
• - Wide QRS complex 
• - Sine wave 

• Treatment 
• - Nebulization with salbutamol 
• - Calcium gluconate - 10% 10ml over 10 minutes
• - 50 ml of 50% dextrose with 10U regular insulin slowly
• - Potassium binding resins 
• - Dialysis

• Magnesium levels should be concomitantly monitored; hypomagnesemia can produce refractory hypokalemia.
• Magnesium is an important cofactor for potassium uptake and for maintenance of intracellular potassium levels.
• In addition, supplemental magnesium reduces the risk of arrhythmia.

• treated with potassium replacement, before their pH is corrected by bicarbonate administration.
• Diabetic patients with ketoacidosis may initially have normal [K+], but hypokalemia rapidly develops asinsulin is administered and as glucose shifts into cells; for suchpatients, potassium supplements should be added to the resuscitation fluid, once the physician is confident that renal function isadequate.
• If hypokalemia develops while patients are undergoing diuretic therapy, additional drugs can reduce the renal loss of potassium

Total serum calcium - 8.5 to 10.5 mg/dL

• Three molecular forms:
• Protein-bound calcium
• Diffusible calcium bound to anions (bicarbonate, phosphate,and acetate), and
• Freely diffusible calcium as iCa2+.

• Normal calcium levels may range from 8.5 to 10.5 mg/day, assuming an albumin level of 4.5 g/dL.
• The calcium concentration [Ca] usually changes by 0.8 mg/dL for every change of 1.0 g/dL in plasma albumin concentration
• Corrected iCa  = Total [Ca] + (0.8 X [4.5 - albumin level])

• Hypocalcemia is defined as total serum concentration below 8.4 mg/dL or ionized calcium concentration below 4.5 mg/dL
• [iCa2+] below 0.8 mEq/liter can lead to central nervous system dysfunction

• Hypoparathyroidism - surgery, autoimmune
• Parathyroid agenesis 
• Magnesium deficiency 
• Tumor lysis syndrome 
• Acute pancreatitis 
• Calcium chelating agents - EDTA, citrate

• Paresthesia 
• Muscle spasm 
• Tetany 
• Seiures 
• Cardiac dysfunction

ECG - Prolonged QT interval, ventricular fibrillation

• Patients with acute symptomatic hypocalcemia  (calcium level < 7.0 mg/dL, iCa2+ level < 0.8 mmol/liter) should be treated promptly with IV calcium.
• Calcium gluconate, preferred to calcium chloride, causes less tissue necrosis if it is extravasated, so it should be given through the central vein route.
• The first 100 to 200 mg of elemental calcium (1 to 2 g calcium gluconate) should be given during 10 to 20 minutes. Faster  administration may result in cardiac dysfunction and even arrest. Those first 100 to 200 mg should then be followed by a slow calcium infusion at 0.5 to 1.5 mg/kg/hr
• The infusion should not contain bicarbonate or phosphate, either of which can form an insoluble calcium salt.
• If bicarbonate or phosphate administration is necessary, a separate IV line should be used.
• Coexisting hypomagnesemia should be corrected in every Patient. Magnesium is given by infusion, initiated with 2 g of magnesium sulfate during 10 to 15 minutes, followed by 1 g/hr.
• Chronic hypocalcemia (hypoparathyroidism) is treated by oral calcium administration and, if that is insufficient, vitamin D supplementation. The serum calcium level should be targeted to about 8.0 mg/dL. If oral calcium preparations cannot achieve adequate calcium repletion, vitamin D should be added. The usual initial daily dose is 50,000 IU of 25-hydroxyvitamin D (or 0.25 to 0.5 mg of 1,25-hydroxyvitamin D).
• If the phosphorus level is higher than 6.0 mg/dL when the calcium level is satisfactory, an unabsorbable phosphate binder should be added.

• Mild hypercalcemia - 10.5 to 12 mg/dL
• Moderate hypercalcemia. - 12 to 14.5 mg/dL
• Severe hypercalcemia - >15 mg/dL
• Hypercalcemic crisis - >: 17 mg/dL, life-threatening cardiac tachyarrhythmia, coma, acute renal failure, and ileus with abdominal distention

• Treatment of the cause – hyperparathyroid adenoma, stop thiazides, malignant excision of tumors,
• Severe hypercalcemia – bisphosphonates (zoledronic acid, pamidronate disodium, and etidronate disodium). Such drugs have a potent capacity to reduce osteoclast-mediated release of calcium from bone. Several formulations of bisphosphonates are available (in order of preference

1.5 and 2.0 mEq/liter

• The most common formulation is magnesium sulfate; 1 g of magnesium sulfate contains 0.1 g of elemental magnesium 8 to 12 g of magnesium sulfate in the first 24 hours followed by 4 to 6 g/day for 3 or 4 days to replete body stores.
• 1 to 2 g of magnesium sulfate as an IV bolus during 5 minutes for torsades de pointes therapy

Serum magnesium > 2.5 mEq/L 

• Causes 
• - Iatrogenic 
• - Advanced renal failure, treatment with magnesium containing antacids. 
• - Diabetes ketoacidosis 
• - Pre-eclampsia (overdose of MgSO4)

• Clinical features 
• - Mild - asymptomatic, Severe - >8 mEq/L
• - Depression of deep tendon reflex
• - Paralysis of voluntary muscles 
• - Hypertension
• - Sinus bradycardia
• - ECG - Prolonged PR, QRS and QT interval

• Treatment -
• - Stop exogeneous magnesium
• - Calcium gluconate
• - Dialysis
• - If normal function, loop diuretics

• o Samples for arterial blood gas analysis must be drawn from an artery into a syringe whose dead space has been filled with heparin. Syringe should not be emptied completely. 
• o Once the sample is obtained, care is taken to eliminate visible gas bubbles, as these bubbles can dissolve into the sample and cause inaccurate results. Sample should be sealed with cork or a cap.
• o If a plastic blood gas syringe is used, the sample should be transported and kept at room temperature and analyzed within 30 min.
• o If prolonged time delays are expected (i.e. greater than 30 min) prior to analysis, the sample should be drawn in a glass syringe and immediately placed on ice.

• Atrial oxygen tension (PaO2) 95±5 mmHg
• Atrial CO2 tension (PaCO2) 40±5 mmHg 
• Atrial O2 saturation (SaO2) 97±2%
• Atrial blood pH (pH) 7.40±0.05
• Atrial blood carbonate (HCO3) 24±2 mEq/L

• • First look at pH.
• • If pH <7.4 or  hydrogen > 40 nanoequivalents, the diagnosis is acidosis. Then look at pCO2. If pCO2 is ≤ 40, do not blame the lungs. It is metabolic acidosis. Figure out the cause and treat it.
• • If pH > 7.4 or Hydrogen < 40 nanoequivalents, the diagnosis is alkalosis. Then look at pCO2. If pCO2 ≥40, do not blame lungs. It is metabolic alkalosis. Most cases can be treated with plenty of potassium chloride 5-10 mEq/hr.
• • If there is acidosis with high pCO2 or alkalosis with low pCO2, then, there is a respiratory problem. If the number of pCO2 and nanoequivalent of hydrogen per liter is roughly the same, the acid-base problem is purely respiratory. Increase ventilation in respiratory acidosis and decrease ventilation in respiratory alkalosis.

1. Normal anion gap - hyperalimentation, addison's disease, renal tubular acidosis, diarrhoea, acetaolamide, spironolactone, saline infusion [@ HARD ASS] 

2. Increased anion gap - Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Infection, Lactic acidosis, Ethylene glycol, salicylate [@ MUD PILES]

1. Calculate anion gap (Normal 12±2 mmol/L)

• 2. Treatment of metabolic acidosis
• - Treat underlying condition 
• - Bicarbonate therapy after primary cause has been addressed. (0.4 X Base deficit X Body weight)
• - Target pH - 7.2, HCO3 - 10mmol/l 
• - One should not attempt to normalize pH with bicarbonate administration because of risk of bicarbonate therapy (Hypernatremia, hypercapnea)

• Vomiting of gastric content 
• Excessive intake of alkaline drugs e.g NaHCO3 
• Cushing syndrome - increased aldosterone 
• Use of diuretics - except carbonic anhydrase inhibitors 
• Severe hypokalemia

1. Correction of volume defecit and hypokalemia. For edematous patients, use acetazolamide. It facilitate fluid mobiliation. 

• 2. Severe alkalemia (HCO3 > 40 mmol/L)
• - NH4Cl - 0.2 X Weight in Kg X [103-serum chlorine in mmol]
• - HCL (0.1N) - 0.5 X weight in kg X [103 - serum chlorine in mmol/L]