Electrolytes, again

Low Na:
– Hypervol: HF/RF/Liver failure/Nephrotic.
Urine Na will be LOW (under 20). Fluid restrict. Diuretics. If severe: Hypertonic saline.
– Euvol:
Urine Na will be high. Fluid restrict 1l/d. Consider demeoclocyline in euvol.

– Dry: (Raised urea with normal or raised creat).
Urine Na will be HIGH (over 20). Treat with N saline.

Urine osmol is over 500 in dry or euvolaemia.

High plasma Na = vol depletion. Ensure no DKA/HONK. Inspidus? Initially treat with N saline 8-hourly.

Low Na:

Na loss –> volume depletion –> ADH released —> water is retained –> even more low Na.
N + V + headache confusion + spasms/cramps/weakness + LOC.

Fluid-heavy: Failures of heart, liver, nephrotic (kidney).
—> Treat or fluid restrict.

Euvolaemic: SIADH! Steroid deficiency! BRAINS! Exclude artefact (lipids or paraproteins).
—> Fluid restrict. VAPTANS.

Dry: Hypovolaemia (vom, diarrhoea), diuretics, Addison’s (gluco + mineralocorticoid def), pain. (Vol depletion –> ADH! —> dry low Na).
—> Correct SLOWLY!

Low potassium = Diuretics/GI loss.
Cardiac monitoring. Under 2.6? KCl, based on renal function.
Low K+ assoc with Low Mg (give Mg So4 – if both low, replace in same bag).

High potassium = Renal failure. Addison’s (morning serum cortisol or short synacthen).

K+ 6.5 = ECG!
– 10ml 10% Ca gluconate over 10 mins.
– 10 Units Actrapid 50ml of 50% Dextrose IV over 10 mins.
– Then: Insulin/Dex infusion. Ca resonium. Haemodialysis. Neb sabs.

Low Ca2++: Renal failure, Vit D deficiency (like Eloise), low PTH.

– If tingling or under 1.5mMl:
10ml 10% Ca gluconate over 10 mins. (low calcium, high potassium = calcium gluconate).
Then bag of Calcium gluconate (40ml of 10% in 500ml N saline 12 hourly?)

– If no sx: Consider IV Mg need. Calichew D3 BD.

High Ca+:
Check PTH. Any thiazides –> high calcium. REHYDRATE & Palmidronate.


ABG – Hi CO2 = Acidosis. Lo CO2 = Alkalosis i.e. co2 is like anti-bicarb.

Site, Size, Shape, Surface, Skin, Scar. Tenderness, Temperature, Transillumination. 
ROME – Resp opp, Metabolic equal. Direction of pH and CO2/HCO3.
Big spleen = Malaria/cMl/Myelofibrosis.

High Anion Gap: KUSSMAL

– dKA
– Uraemia
– Salicylates
– Sepsis
– Methanol
– Alcoholic ketoacidosis
– Lactate.



C – CO/HCN; A – Alcoholic ketoacidosis; T – Toluene


Etyhlene glycol

Normal anion gap – USED CARB – i.e. used up bicarb. RTA/DIARRHOEA/FISTULA!


U = Ureteroenterostomy
S = Small bowel fistula
E = Extra chloride
D = Diarrhea

C = Carbonic anhydrase inhibitors
A = Adrenal insufficiency/Acetazolamide/Addison’s
R = Renal tubular acidosis
P = Pancreatic fistula

Lots of saline can cause hyperchloremic metabolic acidosis with normal anion gap

Not sure about this:

Respiratory if pH is up and Paco2 is down or if pH down and Paco2 is up
Metabolic if pH and HCO3 are both up or if pH and HCO3 are both down
Compensating if Paco2 and HCO3 both up or if pH and Hco3 both are down
Mixed if Paco2 up and HCO3down or if Paco2 down and HCO3 is up

Random O2 bits. Ass-mar

Nasal cannula 2-6L/min. Face mask 5 – 10 L/min

If COPD + abg shows normal pCO2 –> increase sats to 94-98% unless prior hx of hypercapnic respiratory failure.

Sabs –> lower K+.
Ipatropium –> anticholingeric hence causes dry mouth. BEWARE anticholinergics in BPH or Glaucoma.
Steroids suppress adrenals and cause osteoporosis.

Life-threatening asthma: PaO2 under 8, PEF 1/3 of best, sats under 92%, cyanosis.
Near-fatal: Raised PaCo2.

Acute exac: Hi-flow O2; neb sab every 15 mins; neb ipratropium four hrly; pred 40mg or hydrocort 100mg.
Then Mg IV if not responding; consider Iv aminophylline.

Bloods, hyperkalaemia, hypokalaemia.

Normal MCV: Acute loss, ACD.
Low MCV: Iron-def, Thalaessaemia. (Mennorhagia)
High MCV: B12/Folate def.

Neutrophilia = Infection. Infarct. Inflammation. Cancer. Myeloproliferative. Preggers/exercise.
NEUTROPAENIA: Infection/Drugs/Autoimmune/EtOH.

Eosinophilia – Steroids. Asthma etc.
Lymphophilia: CLL/Lymphoma/NO SPLEEN/renal failure–> raised lymphocytes.

Raised platelets:
a) Reactive i.e. cancer, chronic inflammation, no spleen (raised lympho’s and platelets), haemolysis (raised platelets)
b) Cancer: PCV. Myelfibrosis. ET.

Low platelets:
– Infilitration of marrow e.g. by lymphoma, myelofibrosis.
– Nutrients: Low B12/folate –> macrocytic anaemia and low platelets.
– Destruction: DIC/ITP/Infections
– Too much of a spleen – Lymphoma or liver disease causing hypersplenism.

Too much spleen –> low platelets. Too little spleen –> High platelets. Paradoxical buggers, platelets.

– Acidosis releases potassium.
– Renal failure causes high potassium.
– Addisons (adrenocortical deficiency) causes high potassium.
– Digoxin and amiloride cause high potassium.

Big K+: No P wave, prolonged PR interval, broad QRS, peaked T waves. Eventually hyperkalaemia causes sinusoidal. 
Hyperkalaemia = Ca gluconate, Insulin-Dex, Neb Sab, Dialysis

Low K+: Renal or GI loss.
1) Renal loss – RTA, Conn’s (lots of aldosterone).
2) GI loss via D + V (Eloise had LOW POTASSIUM and she is also an asthmatic – sab!)
3) Insulin causes low potassium. Acidosis causes high potassium.
4) Salbutamol

Low Na: Replace no more than 10mMol in a day
High Na: Due to water loss e.g. too many drips, Inspidus, Conn’s (aldosterone!)

Addison’s is reduced adrenocortical drive. Low Na, high K+, high Ca++.
Cushing’s is excess of glucocorticoids (cortisol up). OPPOSITE of ADDISON’S.
Conn’s is excess of aldosterone. Low K+ with normal or high sodium.

Raised urea, normal creatinine = dehydration, GI bleed, high protein diet.
Urea + creatinine up = Renal failure.

CRF –> Causes anaemia of chronic disease, lowered Calcium in chronic renal failure, high phosphate.


Massive haematemesis: H2 receptor antagon – no use in UGI bleed. PPI IV i.e. IV OMEPRAZOLE PPI. Endoscopy. || Angio + tagged red cell scan. Octreotide.

Massive haemoptysis = 100ml to 600m lover 24 horus. 6 units = GI Bleed.
Tx: Lung resection. Ligation.

Haemoptysis: Usually acute bronchitis when <100ml.

Tx: Semi-recumbent, affected side down to prevent aspiration into good lung. Abx. Narcotics for cough suppression.

Pulmonary hypertension
Left ventricular failure
Recurrent pulmonary thrombo-emboli
AV malformations
Pulmonary vasculitis —
Alveolar hemorrhage
Goodpasture’s syndrome (anti-glomerular basement antibody disease)

Haematemesis + maleana = Peptic ulcer i.e. gastric + duodenal (esp. prox duodenum) ulceration (H PYLORI). Oesophageal varices. Gastritis or duodenitis.

USUALLY oesophageal varices 2o to portal HTN. Or GORD. Or duodenal ulcer.

Dyspepsia = duodenal ulcer, gastric ulcer, non-ulcer dyspepsia, reflux oesphagitis, gastric ca, gallstone.

In extremis: O neg.
Band varices. Inject EtOh/Epi. GI bleed –> 6 units!

PUD: H pylori.

Diagnose H pylori: Urea breath test or urease test or antral biopsy.
PPI = Omeprazole. Can cause false negatives hence, stop PPI’s 2 weeks before breath-testing.

Duoedenal (posteriors bleeders – gastroduodenal artery) >>> gastric ulcers.
Pain (dull or burning), several hours after meal, wakes at night. Relieved by food and antacids. Ulcer = very specific location of pain.

Gastric ulcers invaded by splenic artery = torrential bleed.
NSAID’s ===> bleed from gastric ulcer. Esp w nsaids c aspirin.

Antacids (Mg –> diarroea; Al –> constip). Relieve pain. H2 antag: Cimeditine/Ranitidine. RANITIDINE is a H2 antagonist. Omeprazole is a PPI – better than ranitidine. Great if NSAID’s are used. Sucralfate covers the ulcer.

Eradicate H pylori: Special abx + PPI.

DU ulcer > Gastric ulcer (oldies).
DC Barium (gas + barium in stomach).

PEPTIC (DU + GA) ULCERS –> Antacid/H2 blocker (ranitidine)/Omeprazole (PPI). Oi, and eradication too.

If NSAIDs + gastric ulcers –> PPI given together.

UPPER GI BLEED = coffee-ground + malaena. Hcl on blood = coffee ground vom. Tarry black poo = maleana.

Dull donut. Then lean towards you and percuss the dull donut which is now resonant.

[Other signs of ascites may be present due to its underlying etiology. For instance, in portal hypertension (perhaps due to cirrhosis or fibrosis of the liver) patients may also complain of leg swelling, bruising, gynecomastia, hematemesis, or mental changes due to encephalopathy. Those with ascites due to cancer (peritoneal carcinomatosis) may complain of chronic fatigue or weight loss. Those with ascites due to heart failure may also complain of shortness of breath as well as wheezing and exercise intolerance.]

Failures = transudate because they are trans i.e. everywhere. (Transudate via portal vein due to increased portal venous pa. Low protein, low LDH, alkaline, normal glucose.
Salt restrict (lets you diurese) + SPIRO to counter aldosterone. Shunt TIPS.

(Exudates – cancer actively secreting it. Lots of protein, LDH, low pH, low glucose.)
Exudate = cancer. DRAIN OFF.

Ascites cause fluid retention. Can cause SBP.

HF = rise in hydrostatic pressure. Nephrotic/liver failure = Fall in oncotic pressure.
LVF – pulm oedema + pleural effusions.

OEDEMA = Big hydrostatic (e.g. water/Na retention) or low oncotic pressure or increased permeability or reduced lymphatic clearance.

LVH – It’s so big, the L goes onto the right hand side.

Bright red poo = haematochezia = lower GI bleed.
Aspirin is for ARTERIAL stuff. Dalteparin is for VENOUS stuff.
Stop aspirin 7 days pre-op.

LMWH: DVT. Anti-XA. Beware with aspirin – bleeders! Protamine antidote. Check no HIT. Heparin APTT.
Warfarin – Give Vit K to reverse warfarin. Can reverse with PCC or short-lived FFP.

Low insulin: DKA Type I. HONK Type II.

Hyperglycaemia – Dietary indiscretion/DKA/HHS/New onset diabetes. Ppt: MI/Infection/Cocaine/Surgery/Trauma.
DKA – Hyperpneic respirations (fast and deep Kaussmaul respirations). Neurologic symptoms (seizures, focal weakness, lethargy, coma, death) – more prevalent in HHS.

” The Ligament of Treitz which extends from the small intestine at the duodenojeunal junction serves as the anatomic landmark.

Type I = insulin dependent. Beta cells destroyed.
Type II = non-insulin dependent. Insulin resistance.

Upper GIB:
Gastric and duodenal ulcer
Gastritis and esophagitis
Esophageal and gastric varices
Mallory-Weiss tear
Aortoenteric fistula

Lower GIB:
Colitis (infectious, ischemic, inflamma

The presence of clubbing is associated with non-small-cell bronchogenic carcinoma, bronchiectasis, and chronic lung abscess.
The presence of diastolic rumble, with opening snap, loud S1, and loud P2 in the precordial examination, suggest the presence of mitral stenosis.

DM if:

symptoms + 11.1 random
fasting +7
2 hours post 7g OGTT: 11.1

Else impaired fasting/impaired glucose tolerance

Diabetes – Type II:

1. Metformin (reduces gluconeogenesis). Metformin can cause lactic acidosis. Doesn’t cause hypo’s.
2. Glicazide sulphonylurea – hypo’s and weight gain with glicazide but not metformin.
3. Pioglitazone aka thiazolidindediones. Not in HF.

If that doesn’t work —> then insulin. If you have ketosis –> insulin asap!

Glargine/determir = basal long-acting.

ACEi (ramipril)/thiazides/CBB for BP. Statins.
Type I – Insulin! Glargine lantus + levemir determir = Long-acting for basal’s.

Unsorted mess: ECG stuff, ACS, MI etc.

Acute MI = Aspirin 300mg stat. 5mg diamorphine IV. B-blocker IV (continue oral for 1 year). ACEi (if not low BP)
IV fibrinolytics if STEMI LLBB within 12 hours of onset if NOT peptic ulcer, GI bleed, stroke.
Home on: Low dose 75mg aspirin, B-blocker for year, ACEi, statins,

High K+: Flat P-waves, broad QRS, tall t-waves
Low K+: U-wave, prolonged QT. Can result in Torsades.

Hi Ca++: QT shortened, high T-wave.
Low Ca++: ST prolongation.

Digox tox: Sagged ST depressions. Depressed because they’re sagging
like foxgloves.
PE: Deep S in I, Q wave and negative T in III; also negative T in V1-V3. SIQIIITIII for Romans.
RAD. sometimes RBBB.

Pathological Q-wave: Any Q in V1-V3 or otherwise Q waves 2 deep, one wide.
Leads III and AVR = normal to have a Q-wave.

RsR’ and broad QRS, duh = BBB.
PR increased – AV block.
PR reduced (under 120) and delta wave = WPW. Risk of AVRT.

Prolonged QT ==> Low K+. Post MI. Risk of prolonged QT –> torsades –> VF.

AVNRT = Valsava/carotid/adeonine. Narrow tachy.

Broad = over 120ms = VT, SVT with aberrancy, VF.

Brady – any BB, CCB, dig?

LVH = R in V5/V6, S V1 – over 35mm. HTN, AS.

Basis – resus

Pads under right clav + V6 left mid-axillary. 150-200J first shock, then 150-360J subsequent.

VF/VT pulsatile = 30:2. SHOCK! Then restart 30:2. SHOCK! 30:2. SHOCK! 30:2 + Epi 1mg AND Amiodarone 300mg IV. SHOCK! EPI 1mg every 3-5 mins/alternate shock.

PEA30:2. Epi 1mg ASAP. After 2 mins, check. Epi 1mg every 3-5 mins.
Asystole: 30:2. Epi 1mg ASAP. After 2 mins, check. Epi 1mg every 3-5 mins.

Hypoxia/Hypovol/Hyperkal/hypothermia. Tension/Tamponade/Toxins/Thromboembolic.