Applied Physiology
Acid-base
pH = -log10[H+]
Normal range is 7.36 - 7.44
Base-Deficit: Amount of acid/alkali required to restore 1l of blood to a normal pH (at
pCO2 of 5.3kPa at 37'C).
Base-deficit = -[HCO3 - 24.8 + (16.2 x (pH - 7.4))]
Normal ranges





pH: 7.36 - 7.44
pCO2
pO2
HCO3-: 22 - 28
BE -2 +2
Sources of H+
1. Lungs: CO2 + H2O <-> H2CO3 <-> HCO3- + H+
2. Anaerobic metabolism (generating lactic acid from pyruvate)
3. Generation of ketone bodies: acetone, acetoacetate, B-hydroxybutyrate
Sources of Buffer / Bases
1.
2.
3.
4.
Bicarbonate system
Phosphate system
Plasma proteins
Hemoglobin
Organs involved in regulating acid-base balance
1.
2.
3.
4.
Respiratory
Kidneys: HCO control
Blood: plasma protein buffer
Bone
5. Liver: produce HCO3 and ammonia
Acidosis
Alkalosis
Effects
1. Respiratory
o Oxygen: Right shift of curve
(reduced O2 affinity, increased
tendency to oxygenate tissue)
o Pulmonary hypertension
2. Cardiac
o Decreased myocardial
contractility
o Resistance to catecholamines
o Cardiac arrythmias
o Increased sympathetic activity
3. Proteins
o Denatured
Worku
p
1. ABG o
o
o
pH
pCO2
HCO3: Loss from gut,
depletion through buffering,
impaired generation
2. Chloride (chloride retained at expense
of bicarbonate); hypercholraemia
results in low bicarbonate and thus
generates acidosis
o May be due to dehydration
o Can be due to defects in
tubular function
3. Serum lactate: Metabolic acidosis classified by Cohen + Woods
1. Common disorders - liver
disease, renal failure, DKA,
malignancy, short-bowel
2. Drugs/toxins: paracetamol /
salicylate, metformin,
epinephrine
3. Inborn error of metabolism:
pyruvate dehydrogenase
deficiency
o Type A: From Tissue hypoxia anaerobic metabolism of
pyruvate to lactate (any cause
of shock)
o Type B: Not due to Hypoxia
Urine dipstick - ketones
Calculate anion gap (Na + K) - (HCO3- +
Causes:
1. Addition of bicarbonate
o Iatrogenic
o Milk-Alkali
syndrome
2. Loss of chloride (with gain
of bicarbonate)
o Vomiting
o Diuretics
3. Hypokalaemia - shift of
protons into cell
Cl-)
o
Normal Anion Gap: HCO
replaced with chloride ions to
maintain electrochemical
neutrality
1. Addisons (hypoaldosteronism hyperkalaemic acidosis)
2. RTA: - group of conditions that
exhibit renal tubular
dysfunction in presence of
normal GFR
 Type I (distal) - loss of
ability to excrete acid
at CCD; leads to
acidosis
 Type II (proximal) loss of HCO3
resorptive capacity;
leads to acidosis
 Type IV:
Hypoaldosteronism hyperkalaemic
acidosis
3. Ileal conduit
4. Carbonic anhydrase inhibitor
o Increased Anion Gap:
6. MUDPALES - Methanol,
Uraemia, DKA, Paraldehyde,
Alcohol, Lactic acidosis, Ethyl
glycol, Salicylates
Check renal functrion
Action potential
Action potential


Equilibrium potential (of an ion): PD at which ion ceases to flow down
electrochemical gradient (Nernst equation)
Resting membrane potential: PD across cell membrane (calculated by Goldman
equation) - takes into account equilibrium potentials of all ions
Normal cell RMP = -70mV (interior of cell is negatively charged with respect
to exterior)
N/K pump 3/2 helps maintain ionic balance

Action Potential
Rapid change in membrane potential (depolarisation) following a stimulus
with rapid return to resting membrane potential
All-or-none phenomenon
Depolarisation = Na influx (opening of Voltage-gated Na channels)
Repolarisation = K efflux (opening of Voltage-gated K channels)
Ionic balance maintained by 3Na/2K-ATPase
Refractory Period: Period of time after AP that AP cannot be propagated

Myelination
- Increased condution velocity
Saltatory conduction at nodes of Ranvier
Types of Nerve Fibres
1. Group A - largest myelinated
2. Group B - Myelinated autonomic preganglionic
3. Group C - Unmyelinated postganglionic fibres
Drugs affecting neurotransmission
1. Na-channel blockers - LAs
2. K-channel blockers - Tetraethylammonium
Bile
~500mls bile secreted per day in the liver
Secreted into liver canaliculi by hepatocytes
Release stimulated by CCK, gastrin, secretin
Function
1. Emulsification of fat (ADEK vitamins)
2. Aids in absorption
Composition of bile
1.
2.
3.
4.
Water - 97%
Bile Salts - 0.7% - Cholic/Chenodeoxycholic acid
Bile Pigments - 0.2%: bilirubin/biliverdin
Other 2%: Fatty acids, cholesterol, lecithin
Bilirubin / Jaundice
Normal Metabolism
Jaundice Classification
1. Broken down Hb in
Pre-hepatic
reticuloendothelial system
2. Reaches liver bound to albumin
 Haemolytic anaemia
3. Taken up into liver via transporter
 Increased cell turnover 4. Conjugated to bilirubin-Digluconuride
cancer/lymphoma
5. CBili enters bile and into gut and out
into poo
Hepatocellular
6. Small amount enters circulation and
reaches urine / small amount in gut
 Failure of uptake: Gilbert's
converted to urobilinogen and out
 Failure of conjugation: Crigler-Najjar
into urine
 Infections - CMV, Hepatitis
 Autoimmune
Post-hepatic

Investigations in jaundice
1.
2.
3.
4.
5.
FBC
Reticulocyte count
Clotting
LFTS
Virology
Cholestasis / obstruction / biliary
atresia
6. Autoantibody
Calcium Balance
Calcium



Normal level 2.2 - 2.6mmol/l
Distribution: (1) 50% unbound and ionised (2) 40% bound to plasma proteins (3) 5%
associated with anions
99% found in bone
Organ systems regulating control
1. Gut
2. Kidneys
3. Skeletal system
Hormone regulation
Increases Calcium concentration
Reduces Calcium concentration
1. PTH
1. Calcitonin
Produced by parathyroid glands:
o From thyroid
84AA
parafollicular cells:
o Effects:
32AA
3. Bone: stimulates osteoclasts [IL-1] +
o Effects
releases calcium and phosphate into 3.
Bone: Inhibit osteoclast activity
circulation
4.
Kidney: Increases calcium
4. Kidney: (1) increased calcium
excretion
resorption, increased phosphate
loss (2) stimulates 1-alpha-OH
activity of kidney
o
o
Vitamin D
o Formed from cholesterol,
metabolised in liver and kidney
o Effects:
2. Bone: stimulate osteoblast
proliferation
3. Kidney: calcium + phosphate
resorption
4. Gut: Enhances gut absorption of
calcium + phosphate
Hypercalcaemia
Aetiology

Primary
hyperparathyroidism
(adenoma of PTH gland)
Hypocalcaemia

Post thyroid surgery
(removal of parathyroid





Consequences /
clinical features





Malignancy: bronchogenic
carcinoma, secondaries to
bone
Renal calculi, pancreatitis
Renal transplant with
tertiary hyperparathyroidism
Calculi - renal
Increased gastric acid
secretion
Risk of pancreatitis
Constipation
Impairment of tubular
function - polyuria,
polydipsia, dehydration
Tiredness, lethargy,
psychosis
ECG: shortened QT,
increased PR, heart block,
flattened T-waves
glands)



Neuromuscular irritability parasthesia (Chvostek's
facial tap; Trousseau's arm
spasm)
Muscular cramps
Tetany
Acute hypercalcaemia (3.03.5mmol/l)
Management
1. Identify and treat cause
2. Cardiac monitoring
3. Rehydration; to prevent
overload, CVP monitoring;
frusemide for calcium
diuresis
4. Bisphosphonate infusion
(Pamidronate - rapidly
reduce serum calcium)
5. Calcitonin
6. High dose steroids
7. Urgent surgery in cases due
to hyperparathyroidism
1.
2.
3.
4.
Identify and treat cause
Cardiac monitoring
Adequate fluid resuscitation
10ml 10% calcium gluconate
+ 10-40mls in saline infusion
over 4-8hours
5.
Cardiac function
Arterial pressure | Venous pressure | ECG | Cardiac function | Cardiovascular support | Cardiopulmonary bypass
Fluid compartments | Shock | Renal failure | Potassium Balance | Calcium Balance
Thorax | Coronary circulation | Carotid circulation | Blood supply of brain
Cardiac output
Heart rate x stroke volume = 70mls/kg/min (approximately 5l/min)
Cardiac Index
Cardiac output / Body surface area = 2.2-2.5l/min/m2
Cardiac Cycle
Duration 0.8 - 0.9s
1.
2.
3.
4.
Closure of mitral valve (systole)
Opening aortic vavle
Closure aortic valve (forms "dichrotic notch" - outward momentum)
Opening mitral valve (ventricular filling)
EVD = 120mls, ESV = 40mls : Ejection fraction = 80/120 (67%)
In exercise
1. Phases of cycle shorten
2. Ventricular diastole disproportionately shorter - reduced filling time
3. VFT offset by "atrial kick" for more filling
Heart sounds
1.
2.
3.
4.
Mitral / Tricuspid valve closure
Aortic / Pulmonary valve closure
Rapid ventricular filling
Atrial contraction against stiff ventricle
Determinants of Cardiac output
1. Non-invasive
o Pulse, HR, BP, urine output
o ECG
o Echo
2. Invasive
o Oseophageal doppler
o PiCCO - Thermodilution
o Swann-Ganz Pulmonary artery catheter
Multi-lumen balloon-tipped flow-directed catheter; passed through
right heart into pulmonary artery
Reflects Left heart function: - "Wedge" forms continousc column of
blood from left atrium (via lungs)
Indications: (1) inotropic support (2) LV monitoring (3) Multi-organ
failure
Parameters


Direct
1.
2.
3.
4.
5.
Mean arterial pressure
Mean pulmonary artery pressure
Pulmonary artery occlusion pressure
Ejection fraction
Cardiac output - measured using indicator dilution /
thermodilution technique (volume1-temp1 vs volume2temp2)
6. Heart rate
7. Mixed venous oxygen saturation
Derived
1. Cardiac index
2. Stroke volume
3. Systemic vascular resistance
4. Pulmonary vascular resistance
5. Oxygen delivery
Systemic Vascular resistance
(MAP - CVP)/CO X 80 = 900-1400 dyn/s/cm-5
Pulmonary vascular resistance
(MPAP - PAOP)/CO x 80 = 150-250dyn/s/cm-5

Complications of insertion:
1. Any of the central line complications
2. Cardiac arrythmias
3. Valve injury: incompetence of TV or PV
4. Pulmonary artery rupture
5. Pulmonary infarction (if balloon kept wedged too long)
6. Catheter knotting
7. Sepsis
Coagulation
Normal Coagulation / haemostatic function
Depends on
1. Normal vascular endothelium
2. Normal number and function of platelets
o Derived from megakaryocytes in BM
o Release vasoconstrictive 5HT, serotonin, TXA2, ADP
o Bind via phospholipid / vWF to form haemostatic plug
3. Normal amount of coagulation factors
o Forms stable meshwork of cross-linked fibrin around primary platelet plug
(stable haemostatic plug)
4. Essential co-factors - Vit K, calcium
o VitK: Fat soluble leads to carboxylation of factors II, VII, IX, X binding to
surface of platelets
5. Balanced by fibrinolytic pathway
Coagulation pathway
A series of enzyme-controlled steps resulting in the conversion of soluble plasma
proteins (fibrinogen) into insoluble polymerise deposit.
Ie. the formation of a clot!
1. Intrinsic cascade (APTT): components intrinsic to blood itself - clots in tube
(12,11,9,10,2,1)
2. Extrinsic cascade (PT): components activated by extrinsic factors from damaged
tissue (7, 10,2,1)
o Factor VII decays fastest in blood + particularly calcium dependent
Surgical Coagulopathy





Hypothermia - cold results in dysfunctional platelets
Massive transfusion
Aspirin
Heparin (can lead to thrombocytopenia through immunological mechanism "HITS" heparin induced thrombocytopenia
DIC / sepsis
Tests of coagulation
Bleeding Time
Time taken for earlobe to stop bleeding after it's been
punctured
3-5 min. Reflects platelet function
Clotting Time
Time taken for blood to clot in glass tube (intrinsic
pathway)
4-6 min.
Activated Clotting Time
Whole blood clotting time
107seconds + /- 13 seconds
Prothrombin Time
Measure of extrinsic + common pathways
9-15 seconds
Activated Partial Thromboplastin
Time
Measure of intrinsic and common pathways
30-40seconds
Thrombin Time
Measure of common pathway
14-16s
TEG
Dynamic function of everything
TEG (Thromboelastography):
Parameter
Description
Indications
/
Implicatio
ns
R-value
Time from initiation of test to initial fibrin formation
and movement of pin
Coagulatio
n factor
activation
K-value
Time from beginning of clot formation until amplitude Coagulatio
n factor
of TEG reaches 20mm
amplificati
on
Alpha-angle
Coagulatio
n factor
amplificati
on
Max-Amplitude
Greatest amplitude of TEG
Platelet
aggregatio
n
Amplitude at 60mins
Amplitude of TEG 60 minutes after maximal TEG is
recorded clot lysis index
Fibrinolysis
Electrocardiogra
phy (ECG)
Fat / Pulmonary Embolus (PE)
Embolus

Abnormal mass of undissolved material that is carried in the bloodstream from one
place to another
Components of Emboli
1.
2.
3.
4.
5.
6.
7.
8.
9.
Thrombi or mixtures of thrombi and clot
Fat: long bones,
Atheroma - rupture of aotic plaques with emboli to mesenteric vessels
Tumour cells
Air: cannulae, open neck veins, dialysis
Nitrogen: Caisson's disease
Amniotic fluid: labour
Infective: IE
Foreign material - plastic tubing from broken cannulae
Pulmonary Embolus
Trigger/PD
F
Pathophysi
ology
Fat Embolism Syndrome
1. Wall
o
o
Increased ageing
Vessel injury (limb injury)
2. Flow (prolonged stasis)
o Prolonged bed rest
o Recent surgery
o Cardiac failure
3. Constituents
o Polycythemia
o Malignancy
o Dehydration
o Coagulopathy - ProteinC/S, ATIII
deficiency, Factor V Leiden,
Antiphospholipid antibodies,
HRT, OCP
1. Thrombi form in deep veins / right
atrium
2. Propagate
3. Obstruct pulmonary artery (beyond
right ventricular outflow tract)
4. Produces right ventricular strain
5. Reduced blood flow to lung produces
V/Q mismatch (and increased
physiological dead space)
1. Local trauma
o Trauma / long
bone fractures
o Joint
reconstruction
2. Systemic
o Major burns
o cardiopulmona
ry bypass
o Diabetes
o Pancreatitis
1. Mechanical theory
o Damaged
vasculature
releases fat
droplets into
circulation
o Enter
pulmonary
vascular bed
o Enter systemic
circulation via
arterio-venous
shunts
o Impaction of
emboli in
terminal
systemic
vascular beds
produces local
ischaemia and
tissue injury
2. Biochemical theory
o Stress
hormones
released
(steroids,
catecholamine
s)
o Activate
lipases
o Lipases
hydrolyse
circulating
o
Clinical
features
1. Local
o
o
o
Painless/painful swelling or
tenderness of calf
Phlegmasia cerulea dolens ischaemic cyanotic leg following
massive ileo-femoral venous
thrombosis
Phlegmasia alba dolens ischaemic cyanotic leg following
massive ileo-femoral DVT with
arterial spasm
2. Distal
o
Managem
ent
Pulmonary embolism
1. Tachycardia,
tachypnoea
2. Pleuritic chest pain
3. Shock (outflow
obstruction)
4. Right ventricular strain
5. Paradoxial embolisation
(through PFO) leading to
systemic embolisation
1. Prevent
o
o
o
o
o
Early mobilisation
Heparin
TED stockings
Intermittent pneumatic
compression (intraoperatively)
Transvenous intracaval device umbrella + wire filters
2. Treat
o
o
Resuscitate
Investigate
1. ABG - V/Q mismatch
2. Plasma D-dimers
1. FDP from action
lipids into FFAs
and glycerol
FFAs induce
pulmonary
damage and
increase
capillary
permeability
1. Respiratory
insufficiency
o Tachypnoea,
cyanosis pulmonary
vascular
occlusion by
lipid emboli
2. Petechial rash
o Distributed in
area of chest,
mouth, axilla,
conjunctiva direct
embolisation
of cutaneous
vessels
3. Cerebral features
o Encepalopathy
/ distinct
peripheral
weakness microvessel
embolisation
4. Pyrexia, tachycardia,
retinopathy, renal
impairment
o
of plasmin on
fibrin clot
2. Measured by
latex agglutin
test
3. Misses 10% of
PEs
3. ECG
1. Sinus
Tachycardia
2. S1Q3T3
4. CXR - exclude
differentials
5. VQ scan
6. Spiral CT
7. Pulmonary angiography
Specific therapy
1. Thrombolysis Haemodynamically
unstable
2. Pulmonary
embolectomy
3. Anticoagulation:
Heparin + warfarin
Gastrointestinal physiology
GIT
Function
Salivary Parotid
glands Submandibular
Sublingual
Hormones / reflexes Notes

Resection
Saliva (under PNS control)
Amylase
(ptyalin) breaks
 Hypotonic
down
starch into
oligosaccha
rides
Phases of swallowing
1.
2.
Oral (voluntary)
o Bolus
progressively
moved upwards
and backwards by
pressure of tongue
Pharyngeal
o Contraction of
constrictors
o Larynx pulled
upwards/forwards
against epiglottis
(protects airway)
o Upper oesophageal
3.
sphincter relaxes,
superior constrictor
contracts - food
enters oesophagus
o Inhibition of
medullary
respiratory centre
Oesophageal
o Swallowing centre
initiates primary
peristaltic wave
o Relaxation of LOS
(normal pressure
30mmHg)

Stomac
h
Endocrine

Output = 2l/day
Gastric Innervation
Gastrin
(gastric Gcells) of
 Sympathetic: coeliac plexus
fundus:
 PNS: vagus nerve (increased
stimulate
motility)
acid
section,
stomach
contraction,
pancreatic
secretions
Exocrine




Pepsinogen
(precursor
for protein
digestion)
Intrinsic
factor
(gastric
parietal
cells): Aids
resorption
of
B12Water
HCl GPC
1. H+ generated from CO2
(Fundus
dissolving in cytoplasm
predominan
2. Exchanged with K via H/K
tly) ATPase
activates
3. HCO3- generated via
pepsin
dissociation and goes back
Mucous into plasma
necks of
gastric
Acid secretion control
glands in
pylorus
+ ACh (M2): vagus
+ Gastrin : G-cells (fundus)
+ Histamine: Mast cells (Rx ranitidine)
- Somatostatin
- Secretin


Dumping:
early
(osmotic
sucking
effect) / late
(pancreatic
insulin
secretion
following
food)
B12
deficiency
(no IF)
Achlorhydia
(no Fe
absorption)
- CCK
Emptying hormones
1.
2.
gastrin
Phases of gastric acid secretion
(GPC)
CCK +
 Cephalic phase:
secretin
thought/smell/taste - vagal
(duodenum
activity stimulates gastrin
)
secretion/HCl secretion
 Gastric phase: presence of
food - stimulates gastrin and
HCl
 Intestinal phase: presence of
amino acid and food (later
inhibited by release of
secretin and CCK from
duodenum)
Types of contraction



Duoden
um

Iron
absorpti
on
(acidic
environ
ment)


Jejunu
m

Folate
absorpti
on
Ileum

B12
absorpti
on
Bile salt
uptake
Water
resorptio
n


CCK:
stimulates
GB
contraction,
stomach
emptying,
stimulates
pancreatic
lipase
secretion
Secretin:
stimulates
stomach
emptying,
stimulates
pancreatic
secretion
Peristalsis:
Retropulsion - passes food
boluses back
Vomiting [Pyloric stenosis]
Prinicple site to absorption of carbs,
fats, protein, water, electrolytes,
vitamins, minerals
Output = 1.5l/day
Absorbs 8.5l/day
Type of contraction



Segmentation
Peristalsis (localised
contraction)
Pendular movements
(contraction of longitudinal
muscles)


B12
deficiency,
macrocytic
anaemia
Increased
bile salt
production
+ increased
incidence of
gallstones
(Cf Crohn's


Pancrea
s


Endocri (Stimulated by
gastrin)
ne
Exocrine
Output = 1.5L





Large
bowel




Water
absorpti
on
Mineral
absorpti
on
Expulsio
n of
faeces
(Bacteri
al
synthesi
s of vitK
Gastro-Colic reflex
Meal leads to
increased activity of
colon, with increase
in mass contraction
movements
Defecation
1.
2.
Distension
of rectal
walls (from
faeces)
>18mmHg
intra-rectal
pressure
Afferent
impulse
pass to
sacral
segments
(S234)
disease)
Loose/frequ
ent stools
(reduced
water
absorption)
Reduced
Gammaglobulin:
Diabetes
mellitus
Insulin
sensitivity due to
additional
loss of
glucagon
Reduced fat
absorption
(leads to
steatorrhoea
)
Reduced
protein
absorption negative
nitrogen
balance
Reduced
absorption
of Fe and
Ca - due to
loss of
alkalinisatio
n of chyme
in stomach
3.
4.
5.
6.
Stimulates
efferent
reflex +
stimulation
of
thalamus/co
rtical
sensory
areas
producing
consicous
desire to
defecate
Efferent
impulses
back to
myenteric
plexus
activating
PNS
Leads to
contraction
and
expulsion
of faeces +
relaxation
of internal
anal
sphincter
Augmentati
on with
voluntary
contraction
s of pelvic
floor
muscles
Resistance to
defecation - mediated
by pudendal nerve
Involuntary
defecation occurs
when rectal pressure
> 55mmHg due to
contents or spasm.
Fluid compartments / fluid balance
Fluid Compartments of the body
70 kg man is composed of 60% water = 42litres


Intracellular space (2/3): 28L
Extracellular space (1/3): 14L = Plasma (3) + Interstitial (10) + Transcellular (1)
Transcellular fluid includes: ocular fluid, CSF, synovial fluid
NB. Circulating blood volume = 5l (70mls/kg), which is composed of plasma (ECF)
and red cells (ICF)
Input sources



Food: 800mls
Water: 1500mls
Metabolic oxidation: 200mls
Output sources



Urine: 1500mls
Faeces: 200mls
Skin/respiration (insensible): 800mls
Internal water balance
1. Balance between osmolarities of two compartments
2. [Microcirculation]
External water balance (important in Shock)

Reduced circulating volume results in reduction of blood pressure
1. Detected by carotid sinus/aortic arch [high pressure] baroreceptors: Sympathetic
response
o Catecholamine response - vasoconstriction to maintain BP, increase FOC,
increase cardiac output
o Stimulation of B2 adrenoceptors in kidneys kicks off RAS response
2. Decrease in renal blood flow / renal perfusion pressure: Renin-AngiotensinAldosterone response
o B2 stimulation releases renin; converts angiogensinogen to angiotensin I
o angiotensin I converted to angiotensin II by ACE (in the lungs, also degrades
bradykinin)
o Angiotensin II potent vasoconstrictor
o Angiotensin II stimulates the release of aldosterone (from zona glomerulosa)
which promotes Na/water resorption from DCT
3. Stress hormone release - corticosteroids from adrenal cortex
o Salt/water retention
4. Increase in plasma osmolarity: ADH (produced in paraventricular and supraoptic
nuclei) response
o Osmoreceptors detect a rise in osmolarity (from loss of volume)
o Stimulates the release of vasopressin (aka anti-diuretic hormone) - potent
vasoconstrictor
o
ADH (via increase cAMP, aquaporin) stimulates resorption of water from
DCT/CCD
5. Reduced renal perfusion stimulates EPO production (long term)

Increase in fluid volume
1. Distention of cardiac atria [low pressure receptors] - leads to release of ANP:
promotes diuresis
2. Increase in brain naturetic peptide (BNP increased in "cardiac failure")
Assessment of state of hydration
1. Clinical exam
o Skin turgor
o Dry mouth
o Sunken eyes
o Urine concentration
2. Charts
o Tachycardia
o Weights
o Urine output
o CVP measurements
Aim of fluid therapy



Satisfy basal water requirement
Replace fluids lost beyond basal requirement
Support arterial pressure
Agent
Hartmanns
Description
Compound
sodium
lactate
Na
131
Cl
111
N/S
154
154
5% Dex
Dex-Sal
Gelofusin
31
145
31
145
Starch
35g
gelatine
K
5
Ca
2
Lactate
29
pH
5.5
4.0
4.5
6.25
Osm
278
300310
300
Notes
Lactate metabolised to bicarbonate = 278
mosmol/kg
Causes shift in fluids from extracellular to
vascular, thus temporarily replacing lost
blood volume and sustaining blood pressure
until the whole blood can be transfused
154mmol/l
50g dextrose / 1 Litre
40g dextrose
Molecular weight > 30kDa
Chains of glucose
Average Mol weight > 70kDa
Useful in cases of capillary leakage
HAS
4.5% or
20%
Use limited to 1500ml/day – risk of
coagulopathy
Molecular weight 69Kda
Provides plasma expansion + carrier molecule
+ buffer
Dextrans
Colloid composed of branched polysaccharide
t1/2~12h
40 or 70
Dextran 70 reduces platelet adhesion +
interfere Xmatch
Risk of anaphylaxis
Liver
The Liver
30% cardiac output (70% portal vein / 30% hepatic artery from coeliac axis)
Functions of the liver
1. Storage: Vitamin ADK, folate, B12, Ferritin
2. Metabolic
o Carbohydrate - glycogen storage, gluconeogenesis
o Lipid: Ketone bodies, cholesterol, PLs, lipoproteins
o Protein: protein synthesis
3. Endocrine
o Breakdown of steroid hormones
o Vitamin D metabolism
4. Coagulation
o Produces clotting factors
5. Other
o Generates heat
o Breaks down red cells
o Extramedullary haemopoesis
Liver function tests
1. Bilirubin / unconjugated bilirubin
2. Enzymes
o AST, ALT: from injured hepatocytes
o ALP: raised in cholestasis
3. Plasma proteins
o Albumin (alpha fetoprotein is embryonic albumin)
o Globulins
4. Clotting studies
Lung disorders
Atelectasis
Absence of gas from all or part of the lung
Causes
1. Luminal obstruction / hypoventilation - distal gas trapping, gas absorbed (due to
higher partial pressure than mixed venous blood) leading to progressive collapseof
lung beyond obstruction
1. FB: sputum
2. inadvertant endobronchial intubation
3. Upper abdominal/thoracic surgery = reduced lung expansion (from pain,
spliting) leads to retained secretions and distal airways collapse
o High FiO2: (loss of "splinting" from nitrogen mixture, so when oxygen is
absorbed, lung unit collapses)
o Underventilation: hypoventilation leading to progressive absorption of gas
Mural
o Tumour
Extra-luminal
o Compression from pleural effusion / pulmonary oedema
Consequences of atelectasis
1. VQ mismatch and hypoxaemia
2. Reduced lung compliance (smaller airways need more force to open - Laplace)
3. Pre-disposition to infection due to retention of secretions (vicious circle)
Management
1. Pre-operative anticipation
o Chest exercise
o Chest physiotherapy
2. Intraoperative
o Humidified oxygen (improves mucociliary function)
o Adequate tidal volumes - ensures good expansion
o Avoid higg FiO2 (absorption atelectasis)
3. Post-operative
o Sit upright
o Adequate analgesia (facilitates breathing / good tidal volumes)
o Early mobilisation
o Breathing exercises
o CPAP
o
Airway suction
Bronchiectasis

Localised / generalised irreversible dilation of bronchi (as result of chronic
necrotising infection)
Types
1. Follicular: loss of bronchial elastic tissue and multiple lymphoid follicles
2. Atelectatic: Localised dilation of airways associated with parenchymal collapse due
to proximal airways obstructions
3. Saccular
Magnesium balance
Magnesium




Normal levels 0.7 - 1.0 mmol/l
Function - co-factor in enzymes (phosphate transfer), CNS, neuromuscular systems
High magnesium levels prevent calcium cellular uptake
Homeostasis maintained by kidney - freely filtered at glomerulus, reabsorbed at PCT
and TALLOH
Causes of Hypomagnaesemia



Gut loss - diarrhoea / IBD, malnutrition
Renal loss - diuretics
Alcoholism
Microcirculation
1. Capillary filtration pressure
o Length of capillary: 35mmHg at start - 20mmHg at end
2. Interstitial hydrostatic pressure
3. Colloid oncotic pressure (osmotic)
o
o
25mmHg
Exerted by albumin, gamma-globulins
4. Interstitial oncotic pressure
o Exerted by collagen, proteoglycans, hyaluronate
[Oedema][Lymphoedema]
Oedema
Abnormal accumulation of fluid in the intercellular spaces
May be
1. Transudate
o Imbalance in hydrostatic pressures
o Fluid: low protein <30g/l; specific gravity <1.020
2. Exudate
o Inflammatory process
o Fluid: high protein >30g/l; specific gravity >1.020
o Classification - in terms of content or formation: (1) serous - pleural,
pericardial, peritoneal (2) haemorrhagic - TB (3) Purulent - e.coli peritonitis
(4) Fibrinous - pericarditis (5) Pseudomembranous
Classification
1. Exudate
2. Transudate
Motor Control / Muscle contraction
Components of the motor system
1. Cerebral cortex
o Pre-central gyrus (Brodmann area 4)
o Controls contralateral musculuar activity (pyramidal decussation)
2. Subcortical areas
o Basal ganglia
o Brainste
o Cerebellum
3. Spinal cord
4. Motor neurones
o
Alpha motorneurone: large diameter fibre innverating majority of worker
fibre (extrafusal - not encased within connective tissue sheaths)
o Gamma motoroneurone: small fibre innervate intrafusal fibres of muscle
spindle - alters initial lenght of muscle spindle and sensitivity of spindle to
the stretching
5. Motor units
o Consists of motorneurone and muscle fibres it innervates
o Large muscles, large units; small delicate muscles, small units
6. Receptors / afferent pathways
Reflex
Automatic response to a stimulus
Spinal reflex
1. Withdrawal reflex
o Cutaneous nocioception connect to afferent pathway to stimulate alpha
neurones
o Automatic contraction of muscle in response + polysynaptic inhibition of
antagonist muscles
2. Stretch reflex
o Reflex contraction following stretch of fibres
o Mediated by muscle spindle receptors
o Nuclear bag fibres (Group Ia) o Nuclear chain fibres (Group II)
o Patellar tendon stretch reflex:
(1) patellar tendon stretched (2) stretch of quadriceps muscle (3)
spindle fibre stretch (4) afferents discharge back to alphamotorneurone in ventral horn of spinal cord
Muscle Types
1. Skeletal - striated / voluntary
o Type I: Slow twitch, slow fatigue (high concentration of myoglobin) - eg.
soleus
o Type II: Fast twitch, fast fatigue (large reserves of glycogen)
o Calcium binding protein = Troponin
2. Cardiac - striated / involuntary
3. Smooth - voluntary
o Actin/myosin filaments irregularly arranged throughout cell
o Shows spontaneous
o Calcium binding protein = Calmodulin
Skeletal Muscle Contraction
1.
2.
3.
4.
5.
6.
Action potential spreads from motor endplate to T-tubule system
Leads to release of Calcium from Sarcoplasmic Reticulum
Calcium binds troponin C on light chains
Leads to displacement of tropomyosin (removes steric hinderance)
Actin and myosin can cross link
Filaments slide (energy generated from hydrolysis of ATP to ADP)
Cardiac Muscle Contraction





Cardiac cells are mononuclear (multi in skeletal)
Nuclei centrally located
Cardiac muscle fibres are branched
Cardiac cells connected by intercalated disks - contract as syncitium
Larger T-tubule system
1. Rapid depolarisation - Influx of Na
2. Partial repolarisation - closure of VSCC
3. Plateau phase - Slow inward current of Ca
o Myocytes cannot be stimulated to produce tetanic contractions
o Myocytes are non-fatiguable
4. Repolarisation - closure of Ca channels
5. Placemaker potential
o Unstable membrane potentials
o Decay spontaenously to produce AP
o Caused by progressive reduction in membrane's permeability to K
Neurotransmission and Receptors
Receptor
Enzyme coupling (via Gprotein)
Second
messenger
Effectors
Alpha-1
Phospholipase C
IP2 + DAG
Activation of protein
kinases
Alpha-2
Inhibition of adenyl cyclase
Beta 1/Beta
Stimulation of adenyl cyclase
2
Reduced cAMP
Increased cAMP
Activation of protein
kinases
Muscarininc
Nicotinine
- Direct ion channel linkage
Pancreas / Glucose control
Pancreas anatomy
Pancreas


Mixed endocrine / exocrine gland
Secretes 1-1.5l pancreatic juice daily
Function of the pancreas
1. Endocrine
o Alpha cells: Glucagon
o Beta Cells: Insulin
1. Carbs: - Increase glucose uptake, stimulates glycogensis
2. Proteins: Enhances AA into peripheral tissues, stimulates protein
synthesis
3. Fats: Stimulates lipid uptake
4. Potassium: into cells
o [Gamma cells: pancreatic polypeptide - reduces appetite]
o Delta Cells: Somatostatin
2. Exocrine
o 1 - 1.5l pancreatic juice / day
o Aqueous component - water, bicarbonate
o Enzymatic component - digestive enzymes
1. (1) Proteases (secreted as inactive zymogen form) - trypsinogen,
chymotrypsinogen, procarboxypeptidase, proelastase
2. (2) Lipolytic - Lipase, Phospholipase A2
3. (3) Starch digestion - Amylase
Glucose metabolism

Sources
1. Diet
2. Glycogenolysis
3. Gluconeogenesis
o Lactate, glycerol, Amino acids

Blood sugar control
1. Increase BM: Catecholamines, Glucocorticoids, Somatotrophin
2. Decrease BM: Insulin
Ketosis
1. Starvation
o Diabetes - (omission of insulin, infection, drug induced)
o Improper utilisation of TCA components
2. Increased lipolysis and increased FFA production (readily transportable fatty acids
that can be utilised by organs such as heart and brain)
3. Ketone production - acetone, acetoacetate, B-hydroxybutyrate
Postural changes
Standing up
Arterial pressure = HR x SV x SVR
1. Increases venous pooling
2. reduced venous return to heart
3. Reduced stroke volume and cardiac output
4. Reflex sympathetic responses [carotid baroreceptors] ensure maintained blood
pressure
o Reflex tachycardia + vasoconstriction (to maintain status quo)
o Reduction in vagal activity
Postural hypotension
1. Failure to increase HR
o Vaso-vagal
o Fixed heart rate (drugs, heart block)
2. Reduced stroke volume
o Fixed afterload
o Aortic stenosis
o PE
3. Reduced SVR
o Vasodilators
o Sepsis
o Autonomic failure - chronic DM
Potassium Balance
Normal 3.5-5mmol/l
Hyperkalaemia
Causes
Input


Distribution
Excess K therapy
Blood transfusion




Rhabdomyolisis
burns
oncology
Cellular (cf insulin)
Excretion





Consequence: VF arrest
Renal failure
Renin-AngiotensinAldosterone inhibition
(aldosterone
promotes Na
reabsoprtion at
expense of K
excretion)
ACEi
K-sparing diuretics
Addison's disease
(adrenal insufficiency)



> 6.5mmok/l needs urgent treatment (leads to arrest - hence used as cardioplegic
solution)
Symptomatic
ECG changes:
o Tall tented T-waves (T-pot), increased PR
o Wide QRS
o Sinusoidal pattern
Management
1. Recheck potassium
2. Cardiac monitoring
3. Pharmacological treatment
o 10ml calcium gluconate (10%) IV over 2 mins (cardioprotection)
o 20U Insulin + 50ml 50% Dextrose IV (drives potassium into cells)
o Nebulised salbutamol 2.5mg
o Calcium resonium 15g/8hours PO
4. Dialysis (persistently high K / pH <7.2)
Hypokalaemia
Input
Distribution


Decreased oral intake
/ starvation

Alkalosis / insulin
excess
Artefact - sampling
from drip arm
Excretion


GIT losses: vomiting,
diarrhoea, fistula
Renal losses: Conns,
cushings, diuretics,
RTA
Management
1. Replacement
Pulse / Blood pressure
Blood pressure
MABP - Pv = HR x SV x TPR
Systolic pressure = Pressure from force of cardiac contraction
Diastolic pressure = Pressure from resistance arterioles when heart is relaxed
Pulse pressure = Systolic - Diastolic pressure
Mean arterial pressure = Diastolic +1/3Pulse pressure; Eg BP 120/80 - MABP = 93
Systolic
Diastolic Pulse pressure
Exercise
Increased Reduced Widened
Shock
Reduced Reduced Reduced/narrow
MABP
Aortic regurgitation Increased Reduced Widened
Korotkoff sounds
1.
2.
3.
4.
5.
First sound (Systolic pressure)
Louder
Softer
Muffled (used in pregnancy when 5th sound may be "absent")
Silence (Diastolic pressure)
Blood pressure monitoring
Dichrotic notch = momentary rise in arterial pressure on closure of aortic valve
1. Non-invasive
o Sphygmomanometer
2. Invasive
o Direct cannulation of peripheral artery (should perform Allen's test;
competence of collateral ulna arterial circulation - positive if hand still
blanched 15 seconds later)
o Gives continous waveform trace after attachment to electrical transducer
o Complications of art lines: haematoma, digital ischaemia, pseudoaneurysm,
AVfistula, exsanguination
Pulse changes along arterial tree


Occur due to changes in wall stiffness along arterial tree
Radial: higher systolic, lower diastolic, higher PP, lower MAP
Pulses
1.
2.
3.
4.
5.
Anacrotic pulse: slow rise and low amplitude in AS
Waterhammer pulse: Rapid rise and decline in AR
Pulsus Bisferiens: Mixed aortic vavle disease - "double peak"
Pulsus Alternans: Random variation in amplitude of arterial pressure - LVF
Pulsus Paradoxus
o Exaggerated >10mmHg reduction in arterial pressure on inspiration
o Inspiration - reduced intrathoracic pressure - increase venous return increase right sided end-diastolic volume - leads to bulging into left ventricle
reducing size (Bernheim effect)
o Increased pooling of blood in expanded lungs - reduced return to left side of
heart
o Negative pressure transmitted to thoracic aorta
o Effect is reduced pulse pressure
Paradox is (1) audible heart sounds yet (2) no palpable pulse
Causes of Pulsus Paradoxus
6.
Changes in intrathoracic
pressure
o
o
Bronchial asthma
(lung
hyperinflation)
Ventilated patients
(waking off
sedation)
Increased pooling in lungs Reduced return to left side
of heart
o
o
Pulmonary
embolus (+RV
dysfunction)
Asthma
o
o
o
Tamponade
Constrictive
pericarditis
Pneumothorax
Renal Failure
Renal failure
Inability of kidney to excrete nitrogenous / other waste products of metabolism
Develops over hours / days / months
Part of nephron most susceptible to injury = Thick ascending limb of the loop of henle
1. Anatomy - reside in medulla - poorer oxygenation than cortex
2. Metabolism - Active Na/K-ATPase pumps at membrane have high energy demand
Acute Renal failure
Causes
1. Pre-renal
o "Circulatory"- see
cardiac function /
shock / fluid balance
2. Renal
o Acute tubular
necrosis (ATN) Paracetamol
o Glomerulonephritis
o Reno-vascular NSAIDS (blocks
production of
vasodilatory PGE2)
o Hepato-renal
syndrome
3. Post-renal - obstruction
o Luminal: calculi
o Mural:
o Extraluminal: extrinsic compression
from pelvic tumours,
prostatic
hypertrophy,
Abdominal
compartment
syndrome
Pathophysiol
ogy
1. Parenchymal ischaemia ->
reduced perfusion pressure
o Vasoconstriction of
Chronic renal failure
1. Pre-renal
2. Renal
o Congential: PCKD
(extra-renal - cysts in
liver, pancreas, spleen;
berry aneurysms in
circle of bruce willis,
MV prolapse)
o Glomerular: GN,
Diabetes, Amyloid
o Reno-vascular:
hypertension,
vasculitis, RAS
o Tubular/interstitial:
interstitial nephritis,
pyelonephritis
3. Post-renal
o Chronic outflow
obstruction: calculi,
prostatic enlargement,
pelvic tumours
efferent arteriole (to
maintain RBF);
maintains pressure
across Glomerulus
o Results in reduced
blood supply to
tubules from efferent
arteriole and vasa
recta
o Worsens cortical /
medullary ischaemia
2. Tubular ischaemia + necrosis
leads to shedding of cells into
lumen
o Results in luminal
obstruction
3. Promotes "back leak" of
tubular fluid into interstitium
o Increases interstitial
hydrostatic pressure
o Worsens tubular fluid
resorption
Recognition
1. Oliguria
o
<400ml/day urine
2. Reduced GFR
o Raised urea /
creatinine
3. Electrolyte inbalance
o Hyponatraemia
o Hyperkalaemia
o Metabolic acidosis
o Hypocalcaemia
4. Urine composition changes
Complication
s
1. Fluid dynamics
o Acute pulmonary
oedema / fluid
overload
2. Electrolyte balance
o Hyperkalaemia arrythmias
1. Blood results
o trends from previously
2. Signs / symptoms of longstanding disease
o skin pigmentation,
chronic anaemia (lack
of EPO), pruritis,
nocturia
3. USS / imaging
o Bilateral small kidneys
o Scarred kidneys
1. Hypertension
o (RAS)
o Fluid retention
2. Anaemia
o Deficiency in EPO
o Bone marrow fibrosis
(from osteitis fibrosa
cystica)
o Red cell fragility caused
by uraemic toxins
3. Renal osteodystrophy
o Reduced renal
production of 1-alphaOH Vit D
o Leads to hypocalcaemia
and secondary
hyperparathyroidism
(forming bone cysts osteitis fibrosa cystica)
o Reduced bone
mineralisation and
resultant osteomalacia
o Hyperphosphataemia
due to reduced renal
function
4. Uraemia
o From "uraemic toxins"
o Skin pigmentation,
nausea, malaise, itch
5. Neurological
1. Pre-renal
o Optimise filling /
cardiac output
o Careful fluid-balance:
aim for even balance
(fluid charts etc)
2. Renal
o Stop nephrotoxic
drugs (care with
drugs undergoing
renal excretion)
o Manage GN
3. Post-renal
o Catherise
o Monitor urine output
Manageme
nt
Fill
Furosemide boluses (if well filled)
Intropes: Dopamine (increase RBF
+ contractility)
"Renal rescue" - GTN / Dopamine
/ Aminophylline / Frusemide
Optimise nutrition
Renal replacement therapy
Investigations


U/Es
Urine sodium and osmolarity
1. Hypertension
o Loop diuretics
o Fluid restriction
2. Anaemia
o EPO injections
3. Bone disease
o Improve mineralisation
o Vitamin D supplements
o Gut phosphate binders
4. Diet
5. Dialysis/filtration
ATN
Pre-renal failure
- Unable to concentrate urine
- Unable to retain sodium


Urine Na
>20
<40
Urine Osm
<500
>350
Urine:plasma osmolality ratio <1.2
>1.2
ECG
USS kidneys
Renal function
Renal Blood flow


20-25% cardiac output (1 - 1.2 l/min)
Determinants of renal blood flow
1. Autoregulated between 80-180mmHg - (1) Myogenic mechanism: increased wall
tension stimulates vasoconstriction (2) Tubuloglomerular feedback - alterations in
flow of blood occurs with alterations in arterial pressure leading to stimulation of
juxtraglomerular apparatus.
2. SNS: alpha-1 stimulation - afferent arteriole contraction: reduced blood flow
3. Angiotensin II: efferent arteriole constriction (ACEi cause dilation, and reduced blood
flow)
4. PGE2 PGI2: efferent arteriole constriction (NSAIDs cause renal failure by inhibiting PG
production)


Measured by para-aminohippuric acid (PAH): - completely eliminated through
processof filtration and secretion by tbubules (PAH clearance = Renal plasma flow)
Renal blood flow = Renal plasma flow / (1 - Haematocrit)
Renal Clearance



Volume of plasma from which all of a substance has been removed and excreted in
urine per unit time
Clearance = [Urine] x Volume / [Plasma]
Substance
1. Freely filtered (see below)
2. Not secreted / reabsorbed / metabolised
3. Must not inherently alter GFR
Glomerular Filtration Determinants
1. Molecular size - cut off 40Angstroms
2. Molecular charge (BM is negatively charged)
Measurement of GFR
1. Inulin clearance (must undergo continous iv infusion)
2. 24hour urinary creatinine (anhydride of creatine - ie without the water) excretion
(some secretion of creatinine into tubules)
3. 51CrEDTA
Estimation of GFR
1. Cockcroft-Gault formula
The Nephron
1. Glomerulus
2. Proximal convoluted tubule
o Major site of reabsorping solutes (70%): - Na, Cl, K, glucose, amino acids +
phosphate, lactate
3. Loop of Henle
o Resorption of solute (20%): - Na, Cl, K
o Water resorption in thin descending loop (Thich ascending loop is
impermeable to water)
o Forms counter-current mutiplication system - concentrates urine
1. Fluid enters LOH which is isotonic with plasma
2. Decending limb permable to water; water progressively absorbed
down limb (into nephron) making interstitium more concentrated
3. Ascending limb impermeable to water but permeable to sodium passive diffusion of NaCl down concentration gradient, this dilutes
tubular fluid
4. Distal convoluted tubule
o Resorption of solute (10%) - Na, K
o Secretion: variable amounts of K / H
o Reabsorption of water - distal portions
5. Cortical collecting duct
o Water reabsorption (via Aquaporin-mediated V2 receptor: Vasopressin,
produced in supraoptic and paraventricular nuclei, stored in posterior
pituitary)
o Also leads to increased NaCl reabsorption by thick ascending limb - by
increasing concentration of interstitium around loop of Henle.
Glucose and the Nephron


Filtered glucose normally completely resorbed by kidney
Above filtration load, glucose starts to appear in urine (saturated resorptive
capacity)
Respiratory function
Respiratory function | Respiratory failure | Airways Adjuncts | NIV | IV
|
Acid base | PE / Fat Embolus | Pneumothorax | Flail Chest | Chest
drain | Lung disorders
Respiration
Cellular: process of converting glucose into energy (can be aerobic or
anaerobic)
2. Physiological: process of gas exchange
1.
Control of respiration
Cerebral cortex - voluntary control
Brainstem - pons and medulla: autonomic control
o Medullary respiratory centre (Reticular formation)
1. Dorsal group: inspiration
2. Ventral group: expiration
o Apneustic area - prolongs inspiratory phase
o Pneumotaxic area - Inhibits inspiratory area - "fine tunes"
respiratory
3. Chemoreceptors
o Central: ventral surface of medulla - sensitive to PaCO2 (which
diffuses across BBB as H+)
o Peripheral: carotid/aortic bodies - sensitive to PaO2, pH,
PaCO2
4. Mechanoceptors
1.
2.
o
o
Pulmonary stretch receptors (Hering-Breuer inflation reflex distension leads to slowing of inspiration/increase expiratory
time)
J-receptor (located airways close to capillaries) - stimulate
respiration following increase in pulmonary blood flow
Oxygen dissocation curve
Sigmoidal curve: Progressive cooperative binding of oxygen
2. Bohr effect = Right shift of curve
(reduce oxygen affinity)
o Acidosis
o Increased temperature
o DPG
3. Fetal ODC - right shifted (has
higher affinity) to extract maternal
blood
1.
Pulse Oximetry
Measures haemoglobin saturation
and pulse rate
2. Works on principle of
spectrophotometry - differing
amount of light absorbed by
saturated and unsaturated Hb
molecules
3. Sources of error (1) poor
peripheral perfusion (2) unreliable
below 70% sats (3) Ambient light
(4) Nail varnish/pigments jaundice (5) irregular cardiac
rhythms
1.
Gas diffusion
1.
2.
3.
Fluid lining alveoli
Alveolar epithelium
Interstitial space
Basement membrane of capillary endothelium
Capillary endothelium
6. Plasma
7. Red cell membrane
4.
5.
Oxygen delivery
Equivalent to total oxygen capacity of blood x cardiac output
DO2 = [(Hb x sats x 1.34)1 + (0.03 x PaO2)2] x Cardic output = 200ml/L
arterial blood
Oxygen content is determined by
Bound to Hb 99%
o 1.34ml/g oxygen carried by haemoglobin
2. dissolved in solution 1%
o Henry's Law = Gas content = product of solubility and partial
pressure of gas
o Oxygen dissolved = 0.03 x PaO2
1.
Incremental drops in pO2 from the atmosphere to blood
Alveolar-Arterial gradient:


Increased in "lung" pathology- VQ mismatch
Normal in mechanical failure
Alveolar gas equation
PaO2 = PiO2 - PaCO2/R
PiO2 = Inspired PO2
R = Respiratory exchange ration (0.8)
Oxygen therapy
1.
Variable performance
Nasal cannulae
o Face mask (Hudson)
2. Fixed performance
o Venturi mask
o Reservoir bag
o Oxygen tent
o CPAP
o Invasive ventilation
o
Complications of Oxygen therapy
Loss of hypoxic drive
2. Absorption atelectasis (due to loss of splinting)
3. Oxygen radicals
o Direct pulmonary injury - irritates mucosa, loss of surfactant,
progressive fibrosis
o Retinopathy - retrolenticular fibrosis
4. Risk of fire / explosions
1.
Haemoglobin structure





Haem component + 2alpha + 2beta chains
Fe2+ in protoporphoryn ring (Cf Methaemoglobin which is Fe3+ due to oxidation/loss of reducing enzymes)
Can bind total of 4 oxygen molecules (8 atoms)
Also binds: CO2, protons (H+), DPG
Production in (1) Bone marrow (2) Liver + spleen (3) yolk sac in first
few weeks of gestation
Carbon dioxide transport
As bicarbonate: CO2 + H2O -- H2CO3 -- H+ + HCO3o Reaction catalysed by carbonic anhydrase
2. As carbanimo compounds
o formed when CO2 binds with plasma proteins (ie
Haemoglobin)
3. Dissolved in solution (5%)
o CO2 has x24 more solubility than oxygen
1.
Bicarbonate generated increases intracellular osmotic pressure - resulting in
increased venous haematocrit
CO2 can never be expressed as "percentage" saturations as it's solubility is
not saturated!
Haldane effect : Reduced affinity for CO2 in light of increased PaO2
(downshift of CO2 dissociation curve)
Ventilation
Flow of gas per unit time
Minute ventilation = total volume of air entering respiratory tree
every minute = Tidal volume x Respiratory rate
2. Alveolar ventilation = amount of gas entering alveoli each minute =
(Tidal volume - dead space) x Respiratory rate
o More accurate measure of ventilation (only gas that interfaces
with respiration)
o Rapid shallow breaths are inadequate (due to dead space)
1.
Dead space = volume of gas not involved in respiration
anatomical - upper airways not involved in respiration; mouth, nose
etc
2. Alveolar - alveoli ventilated but not perfused (shunts)
1.
Shunt



Perfused but not ventilated
Normal: bronchial circulation, cardiac thebsian veins (drain directly
into left side of heart)
Pathological: Left-to-right cardiac defects (cyanotic septal defects tetralogy)
Pulmonary blood flow
Normal CO - 5-6l/min
Normal Pulmonary artery pressure = 25/8 (pulmonary vascular
resistance is approximately one tenth of systemic vascular resistance
3. Pulmonary Vascular Resistance
1.
2.
falls with rising pulmonary pressure (due to distension of thin
walled pulmonary vessels or to recruitment of collapsed
vessels)
o Increasing radial traction reduces resistance to flow
(poiseulles)
o As lung expands, radial traction forces on blood vessels
increases, increasing calibre
o Controlled by (1) pulmonary artery and venous pressure (2)
Lung volume (3) Pulmonary vascular smooth muscle tone (4)
Hypoxia
4. Blood distribution
o Standing: lowest parts of lungs have greatest flow (hydrostatic
pressure of dependent portions)
o Exercise: Increased upper lobe blood flow
o
Respiratory concepts
Muscles of respiration
o Diaphragm (c345)
o External intercostals
o Accessory muscles - SCM, scalenes, strap muscles
2. Lung
1. Determined by poiseuille's Law
2. Greatest resistance in upper airways, trachea
3. Compliance differs in inspiration and expiration - "Hysteresis"
4. Laplace Law: P = 2T/r; smaller the radius, the more the
tension
5. Increased compliance with bigger alveolar volumes (hence
CPAP)
6. Improved with surfactant (lipid-protein) from Type II
pneumocytes reducing surface tension
7. Decreased compliance with restrictive lung disease, fibrosis
o Airflow
o Compliance: rate of change of volume / rate of change in
pressure = 200ml/cmH20
o Elastance: measure of elastic recoil of lung (1/compliance)
1.
Respiratory assessment
1.
Non-invasive
o Sputum
o Pulse oximetry
o Capnography
o Lung function
1. PEFR
2. Spirometry




Tidal Volume =
7ml/kg = 500mls
IRV = 3L
ERV = 1.3L
RV = Volume
remainin in lung
following maximal
respiration
(measured by helium
Obstructive airways
disease: loss of flow
Restrictive airways
disease: loss of volume

dilution, nitrogen
washout,
plethysmography)
Vital Capacity = 1015ml/kg
Capacity = Sum of two or
more volumes
FRC: Amount of gas
remaining in lung at end of
quiet expiration
Gas transfer
o Imaging
1. CXR
2. CT
3. MRI
4. V/Q scanning
o Echo: assess pulmonary artery pressure and right heart
function
2. Invasive
o ABG
o Bronchoscopy
o Mediastinoscopy - performed via incision at root of neck,
permits biopsies of regional lymph nodes
o Lung biopsy - open / radiologically-guided
3.
Sodium balance
Sodium

Daily requirement: 1mmol/kg/day (cf 0.5mmol/kg/day for Potassium)
Distribution of Sodium in body
1. 50% extracellular
2. 45% in bone
3. 5% intracellular
Physiological role
1. Osmotic effects: internal water balance
2. Generates action potential
Hypontraemia
Hypernatraemia
Classification
1. Water gain
o Increased intake:
polydipsia, binge
drinking, TURP
syndrome
o Increased retention:
SIADH (lung, brain),
cardiac failure,
hepatic failure
2. Sodium loss (water loss)
o Renal loss: Diuretics,
addisons
o Gut loss: diarrhoea,
vomiting
o Other: Burns, DKA
3. Pseudohyponatraemia
o Due to measurement
peculiarities in
presence of
hyperlipidaemia
1. Water loss
o Reduced intake:
o Increased loss:
Diabetes insipidus (lack
of vasopressin - cranial
lack or nephrogenic
insensitivity), osmotic
diuresis
2. Sodium gain (over water)
o Conn's / cushings
o Hypertonic saline
Clinical
features


Management
1. Overload - restrict
2. Losses - replace
Spleen
The Spleen
Features of brain oedema confusion, agitation, fits,
reduced level of
consciousness





Size of a cupped hand; lies 9-11 ribs
Forms left lateral extremity of lesser sac
Ligaments - gastrosplenic, lienorenal
Notched: hilum
Blood supply: splenic artery
Relations




Posterior: left diaphragm
anterior: stomach
Inferior: splenic flexure
Medially: left kidney
Functions of the spleen
1. Filtration - removal of old/abnormal red blood cells, white cells, platelets and
cellular debris
2. Immunological - produces opsonin, antibody synthesis and protection from infection
3. Storage: 35% platelets are stored in spleen
Features in trauma to suspect splenic injury





Direct blunt trauma
Guarded tender abdomen
Low rib fractures (9-11 ribs)
Shock
Shoulder tip pain (phrenic nerve)
Systemic stress response
Stimuli
1.
2.
3.
4.
5.
Trauma
Surgery
Infection
Hypothermia
Hypoglycaemia
Physiological systems involved
1. Sympathetic
o Produces changes in cardiovascular endocrine and metabolic systems
2. Endocrine
o ACTH release: release of cortisol / corticosterone
1. Glucose metabolism
2. Protein uptake into liver, promotion of catabolism
3. Lipolysis
4. Anti-inflammatory, immunosuppressive, anti-allergic
o GH / Somatotrophin
o Glucagon
o Thyroxine
3. Acute phase proteins
4. Microcirculatory changes
Valsalva
Valsalva
Forced expiration against a closed glottis (straining, defecation, coughing)


A test of physiological autonomic function
Therapeutic role in termination of paroxysms of SVTs (increased vagal activity during
phase IV)
Physiological changes
1. Phase I
o
o
Rise in intrathoracic pressure
Transmitted to thoracic aorta - increase in BP
2. Phase II
o
o
Reduced venous return - fall in SV and CO
Fall in CO produced reflex tachycardia
3. Phase III
o Opening glottis, sudden drop in intrathoracic pressure
o Intra-arterial pressure falls as direct pressure on thoracic aorta relieved
4. Phase IV
o Fall in thoracic pressure leads to improved venous return
Non-invasive ventilation
Patent airway/secretion clearing/NGT(decompress stomach)
Minimal monitoring



Saturation probe
ABG/arterial line
Critical care environment
Settings
CPAP
BiPAP


IPAP 10-20 (increase in 5cm increments)
EPAP 5
BiPAP - inspired oxygen unknown due to complex interaction between gas mixing,
site of O2 addition and leakage
CPAP - constant oxygen flow driven
CPAP - Continous Positive Airways Pressure
1. Closed circuit to provide positive airways pressure throught all phases of respiratory
cycle
2. Attached to Tight-fitting mask / ETT
3. Effects
o Recruitment of collapsed alveoli (prevents collapse at expiration)
o Increased FRC (increases volume), improves lung compliance; reduces work
of breathing
o Improves oxygenation
4. Risks:
o Uncomfortable
o Gastric dilation
o Barotrauma to alveoli due to high pressures
Predictors of NIV success
Young age
Lower acuity of illness (APACHE score)
Able to co-operate: better neurological score
Able to co-ordinate breathing with ventilator
Less air leak, intact dentition
Improved gas exchange
Adjunct treatments



Antibiotics
Humidification / saline +/- bronchodilating nebules
Steroids?
Coronary Thrombolysis
Effective if given within 12 hours of pain
Cannot achive re-perfusion in all cases
Limited ability to detect reperfusion
High risk of bleeding
Indications
Contraindications
Presentation within 12 hours of chest pain Haemorrhagic stroke
1. ST Elevation 2mV 2 chest leads
2. ST Elevation 1mV 2 limb leads
3. R-wave + ST depression V1-V3
(posterior infarct)
4. New LBBB
CNS damage / neoplasm
Recent surgery (3/52)
Active internal bleeding
Known / suspected aortic dissection
Known bleeding disorder
Drugs
Streptokinase - takes at least 1 hour to complete (therefore commited to CPR), can
cause allergy/anaphylaxis 1.5MU in 100mls N/Saline
Alteplase (R-tpa): more effective than strep, 15mg iv bolus + 0.75mg/kg/1hour
Reteplase
Tenectplase
Percutaneous coronary intervention PCI
Recommended method for STEMI
Should be achived within 90 min of medical contact
Advantages
1. Reliable re-opening of artery
2. Visual evidence of opening + calibre of vessel
3. Lower risk of bleeding

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