ABC of ABG

ABG [ center]
..
...

:

PH " Power of Hydrogen ".. Changes in H concentration
PO2 = partial Pressure of O2 " Free un bounded O2 NOT
Total O2 " Most of O2 Is Carried on Hb
PaO2 = partial Pressure of O2 in Arterial Blood
SO2 = O2 Saturation in any Blood
" SaO2 = O2 Saturation in Arterial Blood
Pulse Oximeter " Monitor

*************

..
PaCO2
is controlled by Ventilation & the level of Ventlation is
adjusted
to maintain PaCO2 within tight limits by Respiratory
center adjustment
Resp. Center PaCO2

HYPOXIC DRIVE
Chronic
high PaCO2 leads to desensitization of receptors SO
body relies on PaO2
receptors & Decreased PaO2 level becomes the
principal Ventilatory
stimulus >>> Correction by O2 may depress Ventilation
&
increase PaCO2 So O2 must be in acontroled fashion
with ABG monitoring

CO2 COPD
 Resp. Center
- Stimulation -

Hypoxia
When Hb approaches maximal O2 saturation further
increase in PO2 doesn't significantly increase Blood O2
Content
Hb ! O2
Both Oxygenation & CO2 elemination depends on
Alveolar Ventilation SO Impaired Ventilation leads to
DECREASE PaO2 & INCREASE PaCO2
Ventilation Perfusion mismatch & shunting " COLLAPSE
OR CONSOLIDATION " leads to INCREASE CO2
elemination but not INCREASE O2 as Hb is maximally
saturated SO PaO2 & SaO2 is decreased While PCO2
Doesn't increased
CO2
Hb O2
In Type 1 respiratory failure there is LOW PaO2 with
NORMAL or LOW PaCO2 WHILE In Type 2 respiratory
failure there is HIGH PaCO2

*************

Arterial Blood Gases :

? ABG

? Why ABG

To establish a diagnosis " Respiratory failure & Met.

" Acidosis
To assess severity of illness
To guide & monitor the treatment
Acid base balance

! ! H

H is generated from breakdown of fats & sugars this

produces CO2 which dissolves in blood to form H2CO3
H is removed by respiratory system which
removes CO2 , Renal " Metabolic " excretes H in urine &
reabsorb HCO3

H2O + CO2 << -- >> H2CO3 << -- >> H + HCO3

Increased CO2 = Resp. Acidosis & Its decrease = Resp.

Alkalosis WHILE Increased HCO3 = Met. Alkalosis & Its
decrease =Met. Acidosis

*******************

Metabolic Acidosis

Any process that lowers PH other than Increased

Pa CO2 " Accumulation of mat. Acids Excess
Ingestion , Production or Reduced Renal Excretion - or
" excessive loss of HCO3

Hyperventilation is a dominant symptom in Met.

" Acidosis " Resp. compensation

Anion Gap ( Na + K ) ( Cl + Hco3 ) = 10 18 mmol/ L

Gap is made up of un measured anions " phosphate ,

" sulphate & -ve charged Ptn
Rise > 18 mmol/ L = increased un measured anions "
" lactate & salicylates

Lactic acidosis when O2 supply is decreased anaerobic

metabolites " e.g. lactic acid " are increased

= Met. Acidosis with increased anion gap

.... " lactic A. " hyoxia, Shock, Sepses & Infarction
.... " Keto A. " DKA, Starvation & Alcohol Excess
Renal failure .... Poisoning " Aspirin , Methanol

= With Normal Anion gap

Renal Tubular Acidosis, Diarrhea, Ammonium chloride
ingestion & Adrenal insufficiency

*******************

Metabolic Alkalosis
Any process that increases PH other than decreased
Pa CO2 " Increased loss of Cl, K, & Na " e. g. Diuretics "
or sustained Vomiting which leads to H loss
Resp. compensation by increasing Pa CO2 is limited to
avoid Hypoxia
Loss of Cl, K, or Na leads to Retain Na& K by kidney at
expense of H

*******************
= Met. Alkalosis
Vomiting, K depletation, diarrhea , Cushing's & Conn's
Syndrome
Res. Acidosis is increased Pa CO2 leads to
hyperventilation occurs in type 2 Resp. failure or in
met. Alkalosis

Res. Alkalosis is decreased Pa CO2 caused by

hyperventilation or in Met. Acidosis

*******************

Normal values

PH = 7.35 - 7.45
H = 35 - 45 mmol/L
PCO2 = 35 - 45 mmHg in Arterial Blood
PO2 > 80 mmHg in Arterial Blood in room air
HCO3 = 22 - 28 mmol/L
Na = 135 145 mmol/L
K = 3.5 5 mmol/L
Cl = 95 105 mmol/L
Lactate = 0.4 1.5 mmol/L

Hypoxia severity SaO2 " 90 94 % Mild , 75 89 %

" Moderate & < 75 % Sever

Source : Arterial Blood Gases Made Easy



1
Haematemsis & melena.

1st aid measures :-

1-Vital data : pulse .. ... Bl.pr.

2-Canula & give : ((haematemsis cocktail ))

...............> Dicynon"hemostatic" , Konakion "vit.k ", Cyclokabron
" antifibrinolytic" ,and Zantac
" H2 blocker"

3-Ryle --------------- Never before canula

*Values : -Ensure no bleeding
-To wash by cold water with or without adrenaline to cause
local VC.

*Continue wash till it become clear to prepare pt. For endoscopy .

N.B.: Pt. Fit for endoscope means :-
- Ryle wash becomes clear .
- Pt. is not shocked.
- Pt is not in encephalopathy.

4- 3 blood samples ((obtained from the canula before giving

cocktail ))
- One for CBC ----- baseline Hbe
-----Plat. ((decrease in HCV +ve pt. ))
- One for metabolic profile ----Routine ..
- One for blood preparation.
5- ECG ....to exclude ISHD.

** If bleeding severe or pt not fit for endoscope or not available

endoscope
** We may use Sangstakin ---inflate gastric ballon with 250-300 cc
saline
** sangstakin should not be left more than 48 hours to prevent
necrosis .

** Also in case of severe bleeding we can give :-

-Somatostatin:- [Octeriotide = antigrowth hormone] 25-50
ug\h..."one
ampoule contain 100 ug"
- 400 saline or Ringer 4 +
Value : VC.
- Glypressin "One ampoule contain 1mg "
2 6 1

$$. Take care :

It cause coronary VC, so give nitroderm patches if blood
pr. Allows.
Glypressin is # in IHD, old age..
Blood is given if pt. chocked.
Plasma is given if pt INR >1.5
Plat. Is given if pt plat. >50,000
Till blood --give Colloid which last in intravascular space more
than crystalloids. E.g. : Dextran,haemgel.
If Colloid not available ----- give crystalloids E.g.: Saline, Ringer.

II- History taking :

History of :- chronic liver dis., Gu or Du, Drug Intake : aspirin,
NSAID, anticoagulant.

III-Examination: HSM , ascites , flapping tremors.

IV:-Upper GIT endoscope should be done when Pt. becomes fit

for it .
Value : 1- Diagnostic for cause of bleeding
2- Therapeutic ( as mentioned before).
TTT of bleeding Oesophageal varices:

I ) 1st aid measures .

II) Injection sclerotherapy.
III) Anticomato avoid encephalopathy..
*Enema \4 h.
* protein restriction 20gm\d.
* Lactulose 30 cm\3 times\d stopped if diarrhea
*Eradicate bact. Flora :
- Flagyl 250 mg (1*3*7)esp with renal impairment
- Neomycin 500 mg (2*4*5) #with renal impairment.
Side effect : ototoxicity so not given >5days

IV)Guard against SBP by Noroxin (Norfloxacin ) 1*2 .

V) Give (Dicynon ,konakion, Cyclocapron, Zantac) 2 amp\8h.
{ Zantac is # with thrombocytopenia.)

.If bleeding persist we give :-

Sandostatin, Glypressin

After bleeding stopped :

1- follow up GI for injection
.( )
2Drug to decrease portal hypertensionIndral 10mg 1*4
(If Indral can't be given as in case of DM\BAor PVD or CHF)
Give Effox 40 mg 1*2
3- Vit. K (1*3)
4- Liver support Eg: Legalon 1*3
5- Diuretics depend on pt is compensated or not i.e. pt has
ascites.

TTT OF PU

a)1st aid measures

b)Upper GIT endoscopy for D.D.- if active bleeding injection
 with adrenaline
.c) Losec ( Omeprazole) vial + 200 cc Ringer over 2 hours
d) If anteral gastritis or Du Tripple therapy to eradicate h.pylori
It includes :- PPI e.g. : Gastrazole 1*2*15 days
Clarithromycin 2*2*15 days -
.Amoxicilin 2*2*15 days -

-: Discharge Pt. when

Melena stopped
.Hb = 8 or more
Avoid spicy food , smoking , NSAID

.NB: If pt. with PU with severe haematemsis consult Surgery

:Indication of admission of pt
Haematemsis, melena
Tense ascitis
SBP
Hepatic encephalopathy
Recommended pt