Osmolality Goldman

A mole of a substance is the mol wt of that substance in gramsE.g. the mol wt of NaCl is 23+35.5= 58.5Therefore 1mole NaCl = 58.5 g. 1 millimole is 1/1000 of a moleTherefore 1millimole of NaCl is 58.5 mg.The weight of a salt in mg can be converted into millimoles by dividing the weight in mg

by the mol.wte.g. 1g (1000mg) NaCl = 17.1 millimolesMol wt of NaCl =58.5 Therefore 1000/58.5= 17.1Mol wt of glucose C6H12O6 = 12x6 +1x12 +16x6 = 72+12+96=180Osmolality – a Molal solution contains a gram mol wt of the substance dissolved in 1000g

of the solvent(A Molar solution contains a gram mol wt of the substance dissolved in 1 Liter of solvent)It is determined by measuring the depression of the freezing point of a solution,

compared to water, using an osmometer and expressing the value in *C below 0*CThe value can also be expressed in milliosmoles ,using the factor 1000Osm=186*C or

1*C=538mOsmThe normal range of serum osmolality is 275-290mOsm/kg of serum

CASE DISCUSSION Schwartz Pretest Q1

60 yr old healthy male involved in a car accident was admitted to the hospital because of a closed head injury and ruptured spleen.

Pt underwent laparotomy and splenectomy and for the 1st 4 days postop was on IV 5% dextrose in1/4 normal saline at 125ml/hr. Daily output

450-600ml NG drainage and 700-1000ml of urine

Patient is drowsy but easily aroused till the morning of the 5th day when he is found to be in deep coma and by afternoon he begins to have seizures.

What is the most likely cause for the seizures?

What is the treatment?

NORMAL BODY COMP WashMan

Total Body Water- Water makes up 60% of body wt in males (42l in 70kg male)50% in females80% in newborns2/3 is ICF – Intracellular Fluid ( 40%-28L in 70kg male)1/3 is ECF-Extracellular (20% body wt-14I) of which1/4 is Intravascular (plasma 5% body

wt-3.5L) and 3/4 Interstitial(10.5L)Total body water is controlled by ADHSODIUM-85-90% is in ECFChange in serum Na (i.e. Intravascular Na) indicates disturbed water homeostasis and

ICF volumeChange in sodium content ( total body Na) are manifest as ECF expansion (edema) or

contractionOsmolality or tonicity is the solute or particle concentration of a fluid.Solutes that are restricted to the ICF ( K & organic phosphate esters) or ECF (Na & accompanying anions) determine the effective tonicity or osmolality Rule of thumb -Extracellular osmolality = 2x serum Na + 10 Normal body fluid vol and osmolality is maintained by kidneys despite wide variations in

salt and water intake

NORMAL ELECTROLYTE COMP OF IV &IC mmol/L Schwartz

0.75-1.25

2-2.5

22-29

85-115

3.5-4.5

135-145

Intravascular (SERUM)

20

10

HPO4+SO4 150

150

10

ICF

Magnesium (Mg)

Calcium (Ca)

Bicarbonate(HCO3)

Chloride (Cl)

Potassium (K)

Sodium (Na)

ELECTROLYTE

GI –NORMAL VALUES Condon /ACS Manual

20

20

10

10

10

10

5

K

mmol/l

35

35

100

35

25-30

HCO3

mmol/l

45601000-4000

Diarrhoea

1001003500Succus Entericus

751401000Pancreatic Juice

1001401500Bile

1001002000Gastric Juice pH >4

100602500Gastric Juice pH <4

751001000Saliva

Cl mmol/l

Na mmol/l

VOL ml/day

Secretion

1 amp1010006085101401

 Colonic diarrhea

1 amp10400600606010100Ileal fluid

0.25 amp151000101001560Duodenal fluid

0.5 amp5400600251005145Bile

2 amps5600400115355130Pancreatic juice

20700300101020Gastric secretions

550050050530–50Sweat

7.5% NaHCO3 (45 mmol

HCO3–/amp)

 

KCl (mmol/L)

D5W

(mL) 

0.45% Saline (mL)

0.9% Saline (mL)

HCO3–

(mmolL) 

Cl–

(mmol/L) 

K+ (mmol/L) 

Na+ (mmol/L) 

Replacement Guidelines per Liter Lost Current diagnosisAverage Electrolyte Composition

ELECTROLYTES/DAY Wash Man

• Na- usually 50-150mmols. Renal excretion can fall to < 5mmols/d in absence of intake

• K –usually 20-60 mmols when renal function normal

Rule of thumb - Na/K 1mmol/kg/day

• CHO- 100-150 g in the form of dextrose to minimise- protein catabolism& ketoacidosis

• 2-3 l of 1/2N Dextrose Saline (90-125ml/hr)

with 20mmols K/ l

MAINTAINENCE THERAPY Wash Man

500ml - min amount of water req to excrete daily solute load

Solute load of 600mOsm is produced daily by the body. Healthy people can concentrate urine to a max of 1200mOsm/L

• +500ml - insensible loss thru skin, lungs & feces• -300ml- water prod from endogenous metMin water required/day=1000-300ml =700mlRule of thumb - 30 ml/kg/d normal water reqNormally 2-3l water/day to prod 1-1.5L urineCheck daily weight

COMP OF COMMONLY USED IV FLUIDS Condon

22

109

154

154

0

0

0

Cl mmol/L

24

28

0

0

0

0

0

HCO3

mmol/l

19

4

0

0

0

0

0

K mmol/l

2650368Kidral

130274Ringers lactate

15450586DNS

15403080.9%NaCl

0500277850%D/W

010058610%D/W

0502785%D/W

Na

mmol/L

Glucose

(Gm/l)

Osmolality mOsm/Kg)

IV

ABNORMAL FLUID & ELECTROLYTE LOSSES

Wash Manual

1. INSENSIBLE WATER

2. GI

3. RENAL

4. RAPID INTERNAL SHIFTS

5. BLOOD

INSENSIBLE WATER LOSS Wash Manual

From skin and lungs –very variable Inc with inc resp rate, ambient temp and humidity. Inc by 100-150 ml/*C>37* body temp(2ml/kg/*C)

• Sweating- variable 100-2000ml/hr dep on physical activity and ambient temp

Replacement with 5% dextrose or ¼ NS

RENAL LOSSES Wash Manual

• Na losses significant in diuretic phase of ATN, diuretic use,GI losses and catabolic states

• Na retention sig in postop state, dehydration, steroid use• K loss sig in diuretic use, steroid use, GI losses esp.

diarrhoea, ( intracellular shift with Beta agonists like salbutamol)

• K retention sig in high output renal failure, post trauma, blood transfusion

RAPID INTERNAL FLUID SHIFTS Wash Man

• Occurs with peritonitis, burns, intestinal obstruction, sepsis, crush injury

• Need to replace sequestered fluid with normal saline

RENAL FUNCTION Condon

Assessed byUrine sp.gr, pH & osmolality of 1st voided urine in the morning-• sp.gr should be or > 1.016 and pH 5.8 or lower • and urine osmolality should be 850mOsmol/Kg water and ratio of

urine to serum osmolality should be at least 3

<5

10-30

>40

Na mmol/L

15-25Max retention

20-30Conserving

>40Normal

K mmol/LTubular Activity

Anion Gap ACS

• In any biological system in which ions are present , electrical neutrality is maintained by the total # of cations with the total # of anions

• This principal is utilized clinically in patients with suspected acid base disorders by measuring the serum sodium, chloride and bicarbonate concentrations.

• Normally the extracellular conc of Na+ = the extracellular conc of Cl- + HCO3- + a constant designated as delta

Mmol Na = mmol Cl- + mmol HCO3- + Where delta = 8 +/- 4 mmol/l

ANION GAP

• Determination of the anion gap is useful in assessing the etiology of metabolic acidosis.

Mmol Na = mmol Cl- + mmol HCO3- +

Metabolic acidosis can be divided into 2 groups1- with inc Cl ( as in diarrhoea with loss of HCO3)2 with inc of unknown anion as in renal failure where there

is inc sulphate and phosphate,Diabetes ketoacidosis where there is increased ketoacids,Salicylate poisoning where there is inc salicylateLactic acidosis where there is inc lactic acidNa+140mmol / l= Cl 100mmol + HCO3 10mmol + ?

HYPONATREMIA ACS

Caused by• replacing body loss by water alone or 5% dextrose e.g. diarrhoea• Head injury with inappropriate secretion of ADH• Renal disease with inappropriate loss of Na in the urine• Starvation where there is breakdown of muscle with production of salt free

water• Diuretic use especially thiazidesPseudohyponatremia- The serum Na is falsely low because of 1. High serum lipids or protein – Na falls but osmolality stays the same2. If plasma glucose is > 20mmol/L,make a correction• Blood is drawn from an arm with a dextrose dripThe decreased serum Na causes a fall in the osmolality of extracellular comp

and there is movement of water intracellularly causing swelling of cells. This can cause brain edema with inc intracranial pressure

This causes edema, inc in weight, confusion, apathy, weakness, nausea and vomiting.

If not corrected the water excess will progress to muscle twitching, convulsions, stupor and even death as serum Na falls < 120mmol/l

Lab Data

Serum electrolytes(mmol/L)- Na+ 130, K+ 1.9,Cl- 96, HCO3 -19

Serum osmolality: 260mOsmol/L

Urine electrolytes: Na+ 61, K+18

Urine osmolality : 700 mOsm/L

HYPONATREMIA - TREATMENT

• Don't base treatment on serum Na conc alone

• Correct the underlying cause if possible

• With urine osmolality and sodium conc it is possible to come to a diagnosis

HYPERNATREMIAMuch rarer. Caused by• Fever in septic patients• Tube feeding when not diluted with adequate water• Renal disease with loss of solute poor water as in high output renal failure

where there is dec tubular response to ADH• Tracheostomy patients• Nonketotic hyperosmolar dehydration in diabetics secondary to severe

dehydration caused by diuresis and glcosuria• Clinical manifestations is caused by intracellular dehydration. Pt is thirsty,

irritable, restless, disoriented eventually leading to coma, convulsions, and even death as serum Na rises to 160mmol/l

• Brain dehydration leads to dec intracranial pressure causing headache, and when severe can lead to dilatation of intracerebral vessels and eventual tear/ rupture- cerebral hg is frequent finding in pts dying of hypernatremia

• Treatment is giving adequate volumes of water by mouth or as IV 5% dextrose. Correction takes 1-2 days

HYPOKALEMIAThe kidney does not conserve K like NaThere is a constant urinary loss of 40-60 mmol K / dayNormal serum K of 4mmol/l is needed for proper function of muscle- skeletal,

cardiac and smoothSkeletal- muscle weakness, paresthesia, flaccid paralysis when K<3Cardiac- hypotension, bradycardia, arrhythmias, ECG- flat / inverted T waves,

prominent U waves, dep S-T segmentSmooth- decreased intestinal motility, paralytic ileus, abd distentionHypokalemic periodic paralysis- after exercise, heavy CHO mealA deficit of 4-5mmol/l /kg exists for each 1mmol decrease in serum KOnly an emergency when K<2 Can be corrected over 1-2 days If oral is tolerated this is safest – diet rich in

fruits. Check if renal function is normalIV K should not exceed 20mmol/hr in thru a peripheral line at a concentration

not greater than 40mmol/L of normal or ½ normal saline with ECG monitoring

HYPERKALEMIA ACS/WASH MAN/Currentdiag07

Usually ass with renal impairmentCaused by • Metabolic acidosis• Overaggressive K replacement• Transcellular shift- tumour lysis, rhabdomyolysis• Pseudohyperkalemia- due to lysis of RBCs during venepuncture / transportAffects cardiac function- bradycardia, hypotension, vent fibrillation, cardiac arrest as K reaches

7mmol/lECG changes- peaked T waves, prolonged PR interval and widening of QRS complex, loss of P

waves,Emergency which needs rapid treatment-Stop all K Give IV cal gluconate-10ml of 10% soln over 2 min. Immediate, effect lasts1hr 50ml of 50% dextrose + 10 units insulin over 30min K will drop by1mmol/l in 15min and effect

lasts sev hrs HCO3- 3 ampoules in 1litre 5%dextrose if pt not overhydrated FrusemideSalbutamol nebuliser-beta2 agonist therapy. Lowers K by 1mmol in 30min and lasts3 hrsCation exchange resins- retention enema- 50gm in150 ml tapwater or 50gm in 100ml of 20% sorbitol

orally. Lowers K by 1mol in 1hr and lasts 6hrs Dialysis

SHOCK

CAUSES AND MANAGEMENT

DEFINITION

Condition in which arterial blood flow/perfusion (Blood Pressure) is inadequate to meet tissue metabolic needs (perfuse vital organs)

In a healthy adult :Hypotension – arterial BP <90mmHgShock – arterial BP <60mmHgIn elderly even modest fall in BP may result in sig

hypoperfusion of kidneys /brainPostural Hypotension- Drop in Systolic BP of 10-

20mmHg or increase in Pulse Rate of >15 with position change -indicates hypovolemia

Blood & Fluid Loss

in a 70kg patient circulating blood volume is 5 liters(approx 70 ml/kg)-7% body weightPlasma-5%body wt=3,500 mlInterstitial Fluid- 15% body wt = 10,500mlIntracellular volume= 40% body wt= 28,000ml

Loss of Blood15% of blood volume(700-750 ml)- may produce little or no obvious symptoms20% (1000ml) – dizzy on standing – postural hypotension30% (1500ml) –mild tachycardia, tachpnoea and anxiety35%-(1750ml) tachycardia (110-120beats per min) & marked hypotension- shock40% (2000ml) is life threatening

1 ml of blood should be replaced by 4 ml of salineFluid loss-Dizzy on sitting (postural hypotension – 1000ml blood loss /4000 ml fluid loss.

Shock – = 2000ml blood/ 8000ml fluid

•

SHOCK -CAUSES

DIFFERENTIAL DIAGNOSIS OF SHOCK

If BP is unrecordable start basic life support and establish venous access.

Cause of hypotension is often apparent. If not then make a rapid clinical assessment of likely causes

• HYPOVOLEMIA• SYSTEMIC VASODILATATION- SEPSIS, SPINAL

CORD INJURY, VASOVAGAL• ANAPHYLAXIS• OBSTRUCTIVE • CARDIAC PUMP FAILURE

GET HISTORY FROM RELATIVES

RESPONSES IN SHOCK

• Vasoconstriction- noradrenaline, renin –angiotensin,

• Improve cardiac pumping and rate- adrenaline

• Conservation of Fluid- Dec urine- Antidiuretic hormone, aldosterone

• Hyperglycemia -Glucagon

Hypovolemia from Diarrhoea/Vomiting- loss of water & lytes

• Thirsty• Passes small amounts yellow urine• Dizzy on sitting (postural hypotension – 5% body

wt loss =3500 ml Shock – 10% = 7000ml• Cool clammy extremities• Weak or absent pulses• Tachycardia• Decreased tissue turgor- skin folds on pinching it

, sunken eyeballs, tongue has furrows• Empty neck veins in the supine position• Dry axilla & groin ( 1500ml water deficit)

HYPOVOLEMIA

Loss of blood (hemorrhagic shock)

    External hemorrhage •       Trauma •       Gastrointestinal tract bleeding

    Internal hemorrhage •       Hematoma •      Hemothorax or hemoperitoneum • Aortic dissection

  Loss of plasma     Burns     Exfoliative dermatitis

Loss of fluid and electrolytes     External        Vomiting        Diarrhea        Excessive sweating        Hyperosmolar states diabetic ketoacidosis,

    Internal ("third spacing")        Peritonitis, Pancreatitis       Ascites        Intestinal obstruction

Cardiogenic –Cardiac Pump Failure

Myocardial InfarctionCardiomyopathyDysrhythmia     Tachyarrhythmia    Bradyarrhythmia Acute valvular dysfunction

(especially regurgitant lesions)Rupture of ventricular septum or

free ventricular wall

SIGNS & SYMPTOMS OFSHOCK PRODUCED BY PUMP FALURE HEART FAILURE

• Sudden onset in VT/VFib

• Chest pain in MI

• Absent heart sounds or severe tachycardia

• Raised JVP

• Pedal oedema

• Basal lung rales

• Hepatojugular reflux

Obstructive shock-Decrease in Cardiac Filling or Emptying

FILLING

Tension pneumothorax

  Pericardial disease (tamponade,constriction)

  Cardiac tumor (atrial myxoma)   Left atrial mural thrombus

EMPTYING

  Obstructive valvular disease (aortic or mitral stenosis)

Disease of pulmonary vasculature (massive pulmonary emboli, pulmonary hypertension)

SIGNS/SYMPTOMS OF OBSTRUCTIVE SHOCK

RAISED JVP-

• Tension pneumothorax- absent breath sounds

• Cardiac tamponade- distant heart sounds

• Pulmonary embolism- chest pain, dyspnoea, hemoptysis, swollen calf, h/o immobilisation

Distributive shock 

Decrease in Systemic Vascular Resistance - Vasodilatation

  Septic shock    Anaphylactic shock,

  Neurogenic shock

  Acute adrenal insufficiency

Vasodilator drugs

Signs & Symptoms of Septic Shock

Usually gram-bacteria (E.coli,Kleb,Pseuo,Prot.)

Fever with chills,confusion,hyperglycemia

in old/babies, diabetes, immunosuppressed, H/o recent surgery/manipulation of

urinary,biliary,gynae system

ANAPHYLAXISHistory of • Atopy• Insect bite esp wasp/bees• Food (peanuts, fish, eggs, seafood),• Drugs (penicillin, blood products, iron inj,

aspirin, NSAIDS, vaccines

Urticaria, Oedema of skin and mucous membranes

(angioedema),Wheezing- bronchospasmStridor- laryngeal oedemaGeneralised itching, rhinitis, conjunctiva

redness

Neurogenic Shock

Causes–spinal cord injury,spinal anaesthesia, vasovagal- pain/fright- h/o

fainting, bradycardia,

ASSESSMENT OF SHOCK PATIENT

Pt in Cardiac Arrest- call for help

Moniter-

V fib –shock

V tach- vagal manoeuvers- carotid sinus massage

Adenosine-6mg iv fast followed by 5 ml saline flush Rpt in 1-2 min 12mg

Flat line- CPR

ASSESSMENT OF SHOCK PATIENT

Check airway- clear of blood/vomitus Start O2 or intubate if unconsciousAuscultate lungs for air entry absent- tension pneumothorax / hemothorax? (percussion) rales – cardiac failure? rhonchi- anaphylaxis? LVFailureAuscultate heart- distant sounds- cardiac tamponade?Murmurs- acute valve problems?JVP flat- hypovolemia distended- cardiac failure?, PE,,Ten PT,,CardiacTamp?Abdomen- Fullness or pulsatile mass( ruptured aneurysm?) Tender – pancreatitis, perforation?

ASSESSMENT OF SHOCK PATIENT

BP on both arms- different –dissection of aorta

Fever- sepsis

Pt cold clammy- hypovolemia? Cardiac failure?

Hypovolemia signs- skin/tongue turgor, sunken eyeballs, pallor, empty neck veins

Pedal oedema- cardiac failure

Blood around mouth, malena? ( do PR)

Urticaria, wheals, soft tissue swelling (anaphylaxis)

InvestigationsABG ECGCXRBlood tests-Hb,WBC,platelets, Lytes,Blood sugar,

Creatinine, LFT, PT, PTT,Grouping & XmatchCultures- Blood, urine, sputumECHOUltrasound abd , CT head

ASSESSMENT OF SHOCK PATIENT

TREATMENT- HYPOVOLEMIADiarrhoea. Vomiting

Insert 2 IV canulae (16 gauge)-forearm, groin, central line

Cut downHead down positionInfuse normal saline or ringers lactate-

replace ½ the loss Insert Urinary catheter Foley)- 1ml/kgKeep assessing – dec IV when BP >90 and

pt urinating

TREATMENT OF Heart Failure

Myocardial Infarction

MONA

Dopamine

Treatment of Pneumothorax

Insert chest tube in 2nd intercostal space in midclavicular line or

5th intercostal space in mid axillary line

Top of rib

Heimlich valve

Treatment of Sepsis

Antibiotics

Correct cause of sepsis

IV Fluids-leaky capillaries

Treatment of AnaphylaxisAirway- O2 mask/ intubate, / cricothyroidotomy with 14 gauge canula or small

ET tubeHead down if hypotensiveIV lineAdrenaline 0.5 ml of 1:1000 soln IM or 5ml of 1:10,000 soln IV(0.1ml /kg body wt in children) slowly at

1ml/min till Bp recordable rpt every 10min acc to BP/pulseHydrocortisone- 100-300mg IVH1 blocker-Antihistamine- promethazine 25-50mg IV Rpt 4-6hrlyAminophylline IV for bronchospasm (250mg IV)

DOPAMINEActs on diff receptors at diff doses

Low dose- ( 0.5-2 microgm/kg/min) D1 on vascular smooth muscle causes vasodilatation of renal, mesenteric, cerebral, coronary vascular bed

Mod dose (2-5 microgm/kg/min) Beta1 receptors- positive ionotropic and chronotropic

High dose - > 5 microgm/kg/min) Alpha receptors- vasoconstriction and decrease blood flow

Haemodynamic calculations

CVP- = R atrial pressure = 1-7 mm HgPulm art pressure 15-30/3-12 mmHgPAWP= Pulm artery wedge pressure=3-12

mm HgCardiac index = cardiac output 4-6 l/min Body surface area =2.8-3.6l/min/sq.m( sp gr of Hg=13.7)

CASE SCENARIO Schwartz Pretest100

• 20 yr old motorcyclist is struck by a car.

ER evaluation reveals BP of 70/40, heart rate of 140/min

What IV fluid would you start?5%DW, Hartmanns, 0.45%saline, dextran

After infusion of 2L ,BP is 110/70

Which of the following is the best clinical

guide to adequate fluid resuscitation:

1.Urine output > 30ml/hr

2.Pulse rate <100 /min

3.Disappearance of postural hypotension

4.Normal sensorium

5.Normal skin temp

ACID BASE BALANCE ACS

• Enormous amount of acid is produced everyday from daily metabolism

• Oxidation of CHO and fats produce 15,000-20,000 mmols of volatile acid as CO2

• Breakdown of sulphur containing aminoacids and incomplete oxidation of CHO & fats produce 60-70 mmols of fixed acid

• Normally this H+ produced does not change in extracellular pH from its normal value of 7.4(+/-0.2) because of intracellular buffers, pulmonary and renal mechanisms

• Intracellular buffers are phosphates and proteins• Extracellular buffers are haemoglobin, proteins

and the bicarbonate- carbonic acid system

ACID BASE BALANCE ACS

• Normally the body keeps the ph at 7.4 by maintaining the bicarbonate(HCO3) to carbonic acid (H2CO3) ratio at 20 to 1

HCO3 = 20H2CO3 1Increase in the ratio will produce alkalosis ( inc pH)

and decrease will produce acidosis ( dec pH) Carbonic acid behaves as an acid or as the neutral gas carbon dioxide and is expressed by the following equation:

CO2+H2O<->H2CO3 <-> H++HCO3-Where formation of carbonic acid from carbon

dioxide or reversion of carbonic acid to water and carbon dioxide will depend on the acid-base status

ACID BASE BALANCE

H++HCO3- <->H2CO3 <-> CO2+H2OWhen acid is added to the system bicarbonate conc will

decrease with a corresponding drop in the HCO3/H2CO3 ratio <20/1

To combat this ventilation is increased and the newly formed carbonic acid is quickly converted to CO2 and blown off by the lungs, thereby reestablishing the ratio.

If alkali is added to the system the HCO3 increases and the reverse occurs and CO2( and hence carbonic acid) is retained by the lungs through a decrease in ventilation and an increased excretion of HCO3 by the kidneys

ACID BASE BALANCE-ACIDOSIS ACS

Respiratory Acidosis- When normal resp is depressed as in airway obstruction, hypoventilation, pneumonia, pneumothorax, asthma, heavy sedation, emphysema, pleural effusion CO2 is retained increasing Pco2 > 45mmHg, pH decreases. The kidney attempts to compensate by increasing HCO3 absorption and H+ excretion

Patient needs ventilatory assistance- intubation and ventilation to blow off the CO2

Metabolic AcidosisMetabolic Acidosis- Here there is a deficit of HCO3 due to excessive

acid production eg diabetes with excessive ketone formation or • renal disease ( inadequate excretion of inorganic acids like

phosphate and sulphate) or • when there excessive loss of bicarbonate as in diarrhoea,

pancreatic or enterocutaneous fistula or• Lactic acidosis secondary to shock when anaerobic glycolysis

results in accumulation of lactic acid

Acidosis is dangerous as it 1. decreases myocardial contractility causes a reduction in cardiac

output, 2. decreases responsiveness of peripheral vessels to circulating

cathecholamines causing hypotension and 3. increases refractoriness of the fibrillating heart to defibrillation

making cardiac resuscitation difficult

Alkalosis is better tolerated than acidosis and is fact the most common acid base abnormality seen in the early postop period.

This is due to post traumatic aldosteronism stimulated by volume reduction causing retention of Na and HCO3 and secretion of K, hyperventilation secondary to pain and anxiety and nasogastric suction causing loss of acid.

Respiratory Alkalosis- Secondary to hyperventilation usually abates when pain and anxiety subsides. When secondary to hypoxemia it may need ventilatory support. It results in hypokalemia as extracellular K moves intracellularly. Hypocapnea results in cerebral vasoconstriction

Metabolic Alkalosis – results from nasogastric suction with loss of H+.( hypocholeremic, hypokalemic alkalosis) As a result of hypovolemia the kidney reabsorbs Na exchanging it for K and H – thus resulting in acid urine – paradoxical aciduria

ACID BASE BALANCE-ALKALOSIS