General physiologyChapter 1

Adult male – 60%

Adult female – 55%

Infant – 70%

Elderly – <60%

Intracellular fluid (ICF) – 55%

ECF – 45%

Proteins – 18%

Fat – 15%

Minerals – 7%

Plasma

Interstitial fluid

Transcellular fluid:

1–2 L/day

Minimum volume necessary for adequate excretion of toxic waste material is 500 mL

500 mL/day

Evaporation of fluid from skin and airways

Increased in:

Up to 5 L/day

Increased in:

100 mL/day (faecal)

Increased in:

Drink – 1500 mL

Food – 750 mL

Metabolic – 350 mL

Total input – 2600 mL

Urine – 1500 mL

Faeces – 100 mL

Lungs – 400 mL

Skin – 600 mL

Total output – 2600 mL

2 L/day

Sodium – 100 mmol/day

Potassium – 50 mmol/day

First 10 kg – 4 mL/kg/hour

Next 10 kg – 2 mL/kg/hour

Next 10 kg – 1 mL/kg/hour

1 mmol/kg/day

Sucrose is used (called sucrose space) because it moves freely in all compartments and is not degradable

D₂O (heavy water) can also be used

Evan's blue

Serum albumin tagged with radioactive iodine

Inulin

Iron tagged with chromium or phosphate

TBW minus ECF

Plasma volume will fall by 17%, which is survivable

Plasma volume will fall by 58%, which is not compatible with life

Arteriolar end: 32 mmHg

Venous end: 15 mmHg

Arteriolar end: 5 mmHg

Venous end: 0 mmHg

The filtration pressure is more than the oncotic pressure

Therefore fluid moves into the interstitial space

The oncotic pressure is more than the filtration pressure

Therefore fluid moves into the capillary

J_v is the net filtration

K_t is the filtration co-efficient

P_c is the capillary hydrostatic pressure

P_i is the interstitial hydrostatic pressure

s is the reflection co-efficient

p_p is the capillary oncotic pressure

p_i is the interstitial oncotic pressure

R_a is arterial resistance

R_v is venous resistance

Only filtration

No absorption

Only absorption

No filtration

Increased in ventilated patients and during laparotomy

Up to 5 L/day

100 mL/day

Poor water intake

Diabetes insipidus

Decreased total body fluid volume

No clinical dehydration because decreased ECF is balanced by decreased ICF

Increased levels of plasma sodium and urea

Increased infusion of 5% dextrose

Syndrome of inappropriate ADH (SIADH)

Increased ECF is balanced by increased ICF

Decreased levels of plasma potassium and plasma urea

Dehydration

Hypovolaemia

Increased central venous pressure

Cardiac failure

Oedema

Gastrointestinal losses

Diuretics

40 mmol/L

40 mmol/hour

40 ml/hour

Acute renal failure

Increased potassium infusion

Diabetic ketoacidosis

10 ml of 10% calcium chloride (cardiac protection)

15 units of insulin with 50 mL of 50% glucose

10 units of exchange resin (30 g/hour) enema (polystyrene sulphonate)

Fluid exchange is disturbed in:

Limit and localize thrombus

Fibrinolysis and inflammatory reaction

Hormones

Bilirubin

Iron (transferrin)

Copper (ceruloplasmin)

Vitamins (retinol-binding protein)

Drugs

Carriage of CO₂ by venous blood decreases pH by increasing H⁺ ion concentration, but it is buffered by plasma proteins

Complement system

Antibodies (by means of B lymphocytes)

Acute phase reactants, which are increased in acute infection and systemic inflammatory response syndrome (SIRS):

Antithrombin III

Protein C

Protein S

Alpha-2 antiplasmin

Plasminogen inhibitor

For example, the peripheral temperature decreases in hypovolaemia and decreased colloid osmotic pressure

The peripheral temperature fluctuates with changes in either the environmental temperature or the type and quality of clothing being worn

Oesophagus

Rectum

Tympanic membrane

Temperature receptors

Integration and control

Adjustment (behavioural and physiological)

Great veins

Spinal cord

Abdominal viscera

Pre-optic nuclei detect the core temperature

Anterior hypothalamus controls the mechanisms for heat loss

Posterior hypothalamus controls the mechanisms of heat gain by comparing the core and peripheral temperatures and inducing appropriate actions to restore the body temperature to the set point

Seeking shade

Drinking cool drinks

Wearing light clothes to reduce body temperature

Seeking warmth and shelter in cold season

Donning warm clothes to increase body temperature

Regulation of heat loss, mediated by the anterior hypothalamus

Regulation of heat gain, mediated by the posterior hypothalamus

Endotoxins (lipopolysaccharides)

Circulating immune complexes

Tissue breakdown products

Inflammatory mediators

Other pyrogenic stimuli

These act on preoptic hypothalamic nuclei

Synthesis and release of prostaglandin (PG)-E2 follows

Production of cAMP results

The hypothalamic temperature set-point is reset

The body senses that the core temperature is below the set-point (feels cold)

Activation of heat-production mechanisms until body temperature reaches the set-point

When the set point is reset to normal, the body feels hot

Heat-loss mechanisms are then activated until the temperature returns to normal

Exercise

Ovulation

Food (dynamic action)

Increased endocrine activity (thyroid and adrenal medulla)

Malignant hyperthermia (abnormal release of calcium from the sarcoplasmic reticulum to the cytosol in skeletal muscle)

Inhibits the growth of micro-organisms, e.g. pneumococci, anthrax

Increases antibody production

Slows the growth of some tumors

at 41 °C – permanent brain damage

> 41 °C – heat stroke, coma and death

Vasodilators

Vasoconstrictors

Vasodilators

Vasoconstrictors

Vasomotor centre (the medulla)

If the patient is hypotensive, the autoregulation begins to cause an increase in blood pressure up to twice the value within 5–10 seconds

If the patient is hypertensive, the autoregulation begins to cause a decrease in blood pressure up to 1 ½ times the value within 10–40 seconds

Negative feedback

Increase in blood pressure stimulates carotid sinus and aortic arch baroreceptors (pressoreceptors) and the walls of the right and left atria, which are stimulated by stretch

Impulses go through the glossopharyngeal nerve (Hering's nerve) and the vagus nerve to the nucleus of the tractus solitarius and to the vasomotor centre at the ventrolateral medulla

This results in inhibition of the vasoconstrictor centre and a decrease of tonic discharge of the vasoconstrictor nerves, stimulation of the vagal centre and excitation of the vagal innervation of the heart

Results in:

Decreased firing from baroreceptors increases vasopressin and aldosterone and restores ECF volume

The reverse occurs when the blood pressure is decreased

Renin–angiotensin system

Renal regulation of ECF volume

Parasympathetic impulses through the vagus nerve to the heart

Sympathetic impulses through the spinal cord and peripheral sympathetic nerves to all blood vessels of the body

Vasoconstrictor area (C₁)

Vasodilator area (A₂)

Sensory area (A₂)

Effect on the heart

Effect on the adrenal medulla

Carotid sinus

Aortic arch

Solution that contains a weak acid and its conjugate base or vice versa, i.e. conjugate pairs

Function is to minimise any change in pH by rapidly giving up or accepting hydrogen ions

Sum of major cations (Na⁺, K⁺) minus the sum of major anions (HCO₃^–, Cl^–)

Normal: 12–20 mmol/L

If a base is used to achieve neutrality, the sample is acidic, and base excess is reported as negative (−2 or −3)

If acid is used to achieve neutrality, the sample is alkaline, and the base excess is reported in positivity (+2 or +3, etc.)

Bicarbonate:

Proteins

Phosphates

Haemoglobin

Increase in H⁺ ion

Equation moves to right and CO₂ is excreted by lungs

Assisted by renal mechanisms (retention of HCO₃)

H₂O + CO₂ → H₂CO₃ → H⁺ + HCO₃^–

H⁺ goes to tubular fluid (active transport) and HCO₃^– goes to capillaries (diffusion)

H⁺ + (filtered) HCO₃^– → H₂O + CO₂

CO₂ goes back to epithelium and H₂O is excreted in the urine

Filtered HCO₃^– is reabsorbed as CO₂

Increased plasma HCO₃^–

So increased urinary HCO₃^–

Step 3 becomes H⁺ + HPO₄ or NH₃^– in tubular fluid → H₂PO₄ or NH₄ → excreted in urine

In step 4, filtered HCO₃^– goes back to capillaries and increases total HCO₃^–

Reaction as described above

Increase in step 3 and step 4

Decreased H⁺ in plasma

So decrease in HCO₃^– absorption (step 3) and decreased plasma HCO₃^–

p_aCO₂: 5.3 kPa (40 mmHg)

p_vCO₂: 6.1 kPa (46 mmHg)

p_aO₂: 13 kPa (95 mmHg)

p_aO₂: 5.3 kPa (40 mmHg)

pH < 7.35 or > 7.45

pCO₂ < 4.5 kPa suggests respiratory alkalosis if pH > 7.45 or attempted compensation of metabolic acidosis if pH < 7.35 and base excess < −3

pCO₂ > 5.5 kPa suggests respiratory acidosis if pH < 7.35 or attempted 13compensation of metabolic alkalosis if pH > 7.45 and base excess > +3

Base excess is always affected by metabolic acid–base changes

Metabolic acidosis causes base excess < −3

Metabolic alkalosis causes base excess > +3

Rises and falls to original value: dehydration

Sustained rise for 5 minutes of 2–4 cmH₂O: well-filled patient

Rises by > 4 cmH₂O and does not fall again

On great vessels

Lung transplant

Pulmonary embolectomy

Topical cooling

Intra-coronary infusion of cardioplegic solutions that contain K⁺