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Homeostasis
The Interstitial Fluid is the environment of the cells,
and life depends on the constancy of this internal
sea.
Homeostatic Mechanisms : Maintain within a narrow
range.
Tonicity
Volume
Specific ion concentration
Increased Osmolality of ECF
Defence of Tonicity (280-295mOsm/L)
Thirst
Increased
Vasopressin Secretion
Vasopressin secretion
Increased
Inhibitor
Thirst Mechanism
Water Intake
Water Retention
y
Dilution of ECF
Homeostasis
Defence of
Volume:
Angiotensinogen
Renin
Angiotensin I
ACE
Thirst
Adrenal Angiotensin II
Brain
Cortex
Aldosterone
Vasopressin
Kidney
Na Retention
Water
Retention
Blood Vessel
Vasoconstricti
on
Homeostasis
Defence of Specific Ionic Concentration:
Glucose
Na+ & K+
Ca++ - Mainly by Parathyroid & Calcitonin
Mg++ - Incompletely understood mechanisms
Also dependent on H+ ion
pH is maintained within a narrow range.
Base
Excess/
Deficit?
Fixed
Cation
?
Anion
Gap?
Ingestion of
NH4Cl, CaCl2
Strenuous Exercise
Lactic Acid
H
+
io
n
50 - 100 mEq/d
H+ load from
AA
metabolism
Failure of Kidneys to
Excrete PO4--, SO4--
Diabetic
KA
Acidic solution, [H+] > ROOT (Kw), Basic sol, [H+] < ROOT(Kw)
Electrical Neutrality
Mass conservation
Dissociation Equilibrium
Significance:
Includes components of both Met & Resp Acid base disorders
Value of any one variable can be determined if other two known.
Mostly HCO3- is calculated
Dependent
Variables
Constants : Dissociation constants
canDependent
onlyVariables:
be [Hchanged
], [OH ],
[HCO3 ], [CO3 ], [A ], [HA], [H CO ], [CO
by
changing
the
]
independent
dissolved
2-
Hypoproteinemia: Alkalosis
Renal Failure: Accumulation of Phosphate: Acidosis
Clinical Concepts:
Base Excess: Amount of Acid or Alkali required to return
plasma in vitro to normal pH under standard conditions.
Anion Gap:
Clinical Concepts:
Acid Base Equilibrium:
Elimination of Acid
Recovery/Regeneration of Base
Mechanisms that keep pH stable
Buffering
Compensation
Correction
Clinical Concepts:
Buffers:
Definition: A substance that can bind or release H +
ions in solution, thus keeping the pH of the
solution relatively constant despite addition of
large amounts of acid or base.
For Buffer HA,
HA <====>H+ + ApH = pKa + log [A-]/[HA]
Clinical Concepts:
Most buffers are weak acids (Hbuffer) & their Na Salts (Nabuffer)
Strong Acids Buffered by NaBuffer
HCl
Quanitity
pKa
Buffering capacity maximum when pH=pK a
Function well within 1 pH unit. (Eg: HCO 3- - 5.1-7.1)
Clinical Concepts:
Buffers in ECF:
Carbonate-Bicarbonate Buffer
53%
Plasma (35%)
Erythrocyte(18%)
Hemoglobin 35%
Plasma Proteins 7%
Organic & Inorganic Phosphates5%
Buffers in ICF:
Intracellular Proteins
H PO -HPO - system
2
4
4
Intracellular buffers are responsible for ~85% buffering in Met. Acidosis
and ~35% in met alk and almost complete buffering in respiratory
acidosis and alkalosis
Clinical Concepts:
Bicarbonate Buffer:
HCl
Clinical Concepts:
Protein Buffer:
Predominant Intracellular Buffer Large total concentration
pK = 7.4
AA have Acidic & Basic Free radicles
COOH + OH- <====> COO- + H2O
.NH OH + H+ <====> NH + H O
3
3
2
.
Phosphate Buffer:
pK = 6.8
Predominantly Intracellular
Also in renal tubular
HCl + Na2HPO4 <====> NaH2PO4 + NaCl
NaOH + NaH2PO4 <====> Na2HPO4 + H2O
Clinical Concepts:
Compensation:
Pulmonary Compensation
H+ + HCO3-<====> H2CO3 <====>CO2 + H2O
Clinical Concepts:
Renal Compensatoin:
Mechanisms:
1.
2.
3.
4.
RENAL
TUBULAR CELL
HCO + H
3
1.
NaHCO3
2.
NaHCO3
3.
NaHCO3
GLOMULAR FILTRATE
Glutamin
e
2+
Na
H2CO3
CO2
CO2 + H2
O
CO
2
H2PO4-
HCO3- + H+
CA
NH4+
HCO3- + H+
H2O
H2PO4-
NH4+
NH3
Clinical concepts:
Compensation
Prediction
Prediction of
of Compensation
Compensation
Metabolic
MetabolicAcidosis
Acidosis
PaCO
PaCO22==(1.5
(1.5xxHCO
HCO33- -))++88
Or
Or
PaCO
PaCO22will
will 1.25mm
1.25mmHg
Hg(1.0-1.5)
per mmol/L
per mmol/L
in [HCO3-in]
[HCO
Or 3- ]
PaCO2 = [HCO3- ] + 15
Or
PaCO2 = [HCO3- ] + 15
Metabolic Alkalosis PaCO2 will 0.75 mm Hg per mmol/L in [HCO3- ]
Or 2 will 0.75 (0.25-1.0) mm Hg per mmol/L in
Metabolic Alkalosis PaCO
PaCO3-2 ]will 6mm Hg per 10 mmol/l
in [HCO3- ]
[HCO
Or
Or
PaCO22 will
= [HCO
+ 15
PaCO
6mm
per 10 mmol/l
in [HCO3- ]
3 ] Hg
Or
Respiratory
PaCO2 = [HCO3- ] + 15, Max 55mmHg
Alkalosis
Respiratory
Acute
Alkalosis
Chronic
Acute
Respiratory
Chronic
Acidosis
Respiratory
in PaCO2
in PaCO2
Acid-Base Nomogram:
Clinical concepts:
Effect of Temp:
pH rises 0.015/0C drop in temp
Effect of PaCO2 on pH:
Clinical Concepts:
Effect of Electrolytes in Buffering:
Potassium Ion: Intracellular
Sodium Ion
Clinical Concepts:
Role of Bones:
Exchange of Extracellular H + for Na+ & Ca++
Interstitial HCO3-
Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis
Acute
Chronic
Respiratory Alkalosis
Acute
Chronic
Disorder
Primary
Change
Compensa
tory
Change
Metabolic
Acidosis
HCO3_
PaCO2
Metabolic
Alkalosis
HCO3_
PaCO2
Respiratory
Acidosis
PaCO2
HCO3_
Respiratory
Alkalosis
PaCO2
HCO3_
Acidosis:Clinical Effects
CVS:
Combination of Effects of Direct depression and Catecholamine
stimulation
Heart Rate: Initial Increase then Decrease
Rhythm: Increased Atrial & Ventricular Dysrrhythmias
Due to Changes in S K+
Lower threshold for VF
Increased Catecholamines,
Decreased Arterial tone,
Increased Venous Tone
At <7.0, Decreased d/t direct depressant effects
CCF d/t Increased venous tone.
Acidosis:Clinical Effects
Vascular Effects:
Direct Vasodilatation
Vasoconstriction d/t Catecholamines
Airway Resistance:
Pulmonary Vasculature:
RR
Vasoconstriction
Enhanced HPV
Renal System
Vasoconstriction
Uteroplacental:
More with RA
Impaired central regulation
Cutaneous vasodilatation
Decreased Cellular Metabolism
Direct
Indirect
Clinical
Heart rate
Cardiac inotropy
Airway tone
Ionised calcium
Serum potassium
Respiratory Acidosis:
Primary Increase in PaCO2
Cause:
Production/ Elimination
Produced by:
Elimination by Lungs.
Immense capacity
CO2 - ventilation compromised
Respiratory Acidosis:
Causes:
Alveolar
Hypoventilation
CNS Depression
Drugs
Cerebral Ischemia/trauma
Sleep Disorders
Pickwickian Syndrome
Neuromuscular
Disorders
Neuropathy
Myopathy
Kyphoscoliosis
Flail Chest
FB/Tumor
COPD/Sever
Asthma
Pneumothorax
Pleural Effusion
Airway Obstruction
Pleural Abnormality
Pul edema/embolus
Pneumonia
ILD
Ventilator Dysfunction
Respiratory Acidosis:
Causes Contd
Increased CO2 Production:
Respiratory Acidosis:
pH 7.36
PaCO2 64
HCO3- - 33
pH is acidic, but normal
PaCO2 > 40 => Resp Acidosis
Compensation expected:
HCO3- = 24 + (64-40) x 0.1 = 24+2.4 = 26.4 or
24 + (64-40) x 0.4 = 24 + 9.6 = 33.6
Diagnosis: Chronic Respiratory Acidosis
Metabolic Acidosis:
Causes:
Increased Anion
Gap
Increased
Production of
Endogenous Acid
Ketoacidosis- DM,
Starvation
Lactic Acidosis
Mixed- NKHC, Alcoholic
Abnormal AA Met.
CRF
Ingestion of Toxins
Salicylate
Methanol
Ethylene Glycol
Paraldehyde, Toluene,
Sulphur
Rhabdomyolysis
Metabolic Acidosis:
Causes Contd
Normal
AG(Hyperchloremic)
GI Loss of HCO 3
Diarrhea
Fistula- Pancreatic,
Biliary, Small Intestinal
Ureterosigmoidostomy
Obstructed Bowel Loop
Cholestrylamine, CaCl2,
MgSO4
RTA
CA Inhibitors
Hypoaldosteronism
Dilutional-
TPN
NH4Cl, Lysine
hydrochloride,
Arginine
Hydrochloride
Metabolic Acidosis:
pH 7.36
PaCO2 26
HCO3- - 13
BE - -11
pH Acidic but normal
PaCO2 Decreased => Not Respiratory
Treatment:
Acute Respiratory
Acidosis
Chronic Respiratory
Acidosis
Indications
Carbicarb, THAM
Treatment:
Problems with Bicarbonate Therapy
Intracellular Acidosis
CSF Acidosis
Rebound Alkalosis
Alkalosis:
Physiologic Effects:
1. Left shift of ODC
2. Hypokalemia
3. Low ionised Ca++
4. Decreased CBF
5. Depressed
Ventilatoin
6. Respiratory Alkalosis
Bronchoconstriction
Decreased PVR
Effect
Dire
ct
Indir
ect
Clinic
al
Cerebral BF
Heart rate
Cardiac
inotropy
Systemic Art
tone
Syst venous
tone
PA tone
Airway tone
Uterine BF
Renal BF
Ionised Ca++
Central Stimulation
Pain
Anxiety
Ischemia
Tumor
Infection
Fever
Drugs: Salicylates,
Progesterone,
Doxapram
Peripheral
Stimulation
Unknown
Hypoxemia
High Altitude
Pulmonary Disease:
CHF, NCPE, PE, Asthma
Severe Anemia
Sepsis, Metabolic
Enceph
Iatrogenic:
Ventilator Induced
Respiratory Alkalosis:
pH 7.5
PaCO2 35
HCO3- - 22
pH Alkalemia
PaCO2 Decrease => Respiratory Alkalosis
Expected Compensation: 24-(40-35)x0.2 = 23 or
24-(40-35)x0.4 = 22
Diagnosis: Chronic Respiratory Alakalosis
Respiratory Alkalosis:
Treatment:
Metabolic alkalosis:
Causes:
ECF Contraction,
Normotension,
K+ Deficiency & 20
Hyperreninemic
Hyperaldosteronism
Gastrointestinal
Vomiting
NG suction
Villous Adenoma
Renal
Diuretics
Mg++ Deficiency
Chronic Hypokalemia
Hypercalcemia/Hyperp
ara.
Post Hypercapnic State
Barters syndrome
Sweat
Cystic Fibrosis
Metabolic alkalosis:
Causes:
ECF Expansion,
Hypertension, K+
Deficiency &
Mineralocorticoid Excess
High Renin
Low Renin
Other
Liquorice
Milk-Alkali Syndrome
Metabolic Alaklosis:
pH 7.58
PaCO2 48
HCO3- - 44
BE - +19
pH Alkalemia
PaCO2 Increased => Not Respiratory
Metabolic Alkalosis:
Treatment:
Acetazolamide
Alkalosis:
Anaesthetic considerations:
PO2 90.6
PCO2 53.8
pH 7.484
K+ - 3.7
Na+ - 151
HCO3- (A) 37.7
BE 13.9
SBE 14.1
SO2 97.3
pH Alkalemia
PCO2 Increased =>
Metabolic Alkalosis
Expected Compensation:
PaCO2 =
40+(13.7x0.75) = 50.2
Body never
overcompensates
Diagnosis:
Metabolic Alkalosis +
Respiratory Acidosis
Summary:
References:
Thank