WEEK 1 Flashcards
The neck is essentially composed of vertical columns surrounded by fascial sheets with potential spaces between. Describe the columns & fascia in detail.
- Neuro-musculo-skeletal column with prevertebral (base of skull to ligs at T3) fascia 2. Visceral column with pretracheal (from hyoid to fuse with pericardium) & buccopharygeal fascia 3. Carotid NVB with carotid sheath on each side Everything is surrounded by the layer of INVESTING FASCIA (which splits to enclose trapezius & sternocleidomasteoid muscle)
Describe the concept of the anterior and the posterior triangles of the neck, and their boundaries

Where do the internal & external carotid arteries begin & end? Where does the common carotid bifurcate?
sternoclavicular joint to the transverse process of the atlas (midway between mastoid & angle of mandible)
at C3/4 or the upper edge of thyroid cartilage
Where is the internal jugular vein found?
deep to sternocleidomastoid, but superficial to the common and internal carotids - therefore visible as the (raised) jugular venous pulse wave
Where is the (i) cutaneous cervical plexus (ii) accessory nerve located? What does the accessory nerve supply?
Emerging posterior to sternocleidomastoid and passing adjacent to the external jugular vein
passing across the posterior triangle to supply trapezius
What are the internal & external jugular veins accompanied by?
Superficial & deep cervical lymph nodes
What is the path of the internal jugular vein - with reference to the internal carotid artery.
As the IJ Vexits the skull from the jugular foramen, it lies posterior to the internal carotid artery
It is then lateral to the artery for most of its course
But is anterior to the artery at its termination
Where is the external jugular located? What is it used for?
Just below & behind the angle of the mandible, to mid clavicle
more or less vertical, superficial to sternocleidomastoid
May be used for venous access (particuarly in babies)
What is meant by the term “functional syncitium”?
Cells of atrial myocardium are all electrically connected. They depolarise & contract synchronously.
The ventricles have a similar structure but are a separate functional unit
What is the process of electrical conduction at intercalated discs and the principles resulting in “pacemaker” activity?
About 1% of cardiac fibres do not contract, but form the excitatory & conductive muscle fibres
SAN = the intrinsic pacemaker , BUT other areas do have pacemaker ability
With regards to SAN depolarisation, what does (i) sympathetic (ii) parasympathetic nerves do to its rate?
(i) increases rate of SAN depolarisation
(ii) decreases rate of SAN depolarisation
Describe the 5 phases involved in atrial/ventricular depolarisation. (HINT: THE FIRST IS PHASE 0)
PHASE 0 - rapid depolarisation due to an increase in Na permeability (gNa) as fast Na channels open
PHASE 1 - start of repolarisation as fast Na channels close
PHASE 2 - effect of Ca entry via L-type channels
PHASE 3 - rapid repolarisation as increase in intracellular Ca stimulates K channels to open & gK increases. Ca L type channels close
PHASE 4 - stable resting membrane potential where gK exceeds gNa by 50:1

What are the 3 phases of SAN depolarisation? Describe them.
PHASE 1 - a gradual drift increasing in resting membrane potential due to an increase in gNa as “funny” F-type Na channels open & decreases gK permeabiility as K channels slowly close. “pacemaker potential”. Transient (t) Ca channels help with the “final push”
PHASE 2 - moderately rapid depolarisation due to Ca entry via slow (L) channels
PHASE 3 - rapid repolarisation as elevated internal Ca stimulates an opening of K channels and an increase in gK

How do the sympathetic and parasympathetic nerves modify the spontaneous electrical activity of the heart?
SYMPATHETIC: NA acts on beta1 receptors to increase cAMP production. It increases the rate of SAN phase 1 depolarisation, which increases gCa & gNa “funny” channels
SHOWS +VE CHRONOTROPIC EFFECT
PARASYMPATHETIC: ACh on M2 receptors which decreases cAMP production . It reduces the rate of phase 1 depolarisation. Hyperpolarises membrane potential to lower starting level which increases the extent & duration of opening of potassium channels which increases gK
SHOWS -VE CHRONOTROPIC EFFECT
What are the rates of depolarisation of (i) SAN (ii) AV node (iii) Bundle of His (iv) Purkinje fibers (v) Ventricles?
(i) 90/min
(ii) 60/min
(iii) 50/min
(iv) 40/min
(v) 30/min
What is the intrinsic pacemaker?
The SAN as it has the fastest rate
What happens if conduction is blocked?
Downstream tissues assume their intrinsic rate
What does an Electrocardiogram (ECG) measure? How many electrodes are used and where?
Measures electrical activity of the heart over time
Uses multiple electrodes:
- 4 on the limb : ones an “earth”, used to remove background noise noise & the other 3 are used to create virtual “leads” between each pair of electrodes
- 6 across the chest: to give more sepcific, localised information about areas of the heart
What 2 things do the limb leads measure? What causes the trace to go (i) up (ii) down?
They measure the sum of the electrical activity of the heart & the direction that the electrical activity is moving in
- one end of each lead is designated “positive”
depol moving TOWARDS the positive causes the trace to go UP
depol moving AWAY from the positive causes the trace to go DOWN
What 2 things determine the size of electrical signals from the heart?
current (proportional to tissue mass)
direction of signal
What is the equation for calculating the observed signal? Explain what each symbol stands for.
Observed signal = E x Cos (theta)
the smallest angle gets the biggest observed signal
E = electrical event
theta = angle between the event & ECG lead
With regards to an electrocardiogram, what is the (i) P wave (ii) QRS wave (iii) T wave?
(i) atrial depolarisation
(ii) ventricular depolarisation
(iii) ventricular repolarisation

What are the timing intervals for (i) P-R interval (ii) QRS complex width (iii) Q-T interval?
(i) 0.15 - 0.2s
(ii) 0.08 - 0.12s
(iii) 0.25 - 0.35

How is force is produced in cardiac muscle? How does this differ from skeletal muscle?
An AP causes L-type dihydropyridine channels to open resulting in a large influx of calcium from outside of the cell (only about 10% of this contributes to contraction)
Cardiac muscles T tubules are 5x greater in diameter than skeletal (=> 25x greater volume)
Cardiac t-tubule mucopolysaccharides sequester Ca2+
DHP activation causes release of Ca from sarcoplasmic reticulum via ryanodine release channels
At resting HRs, intracellular Ca conc increases due to influx & sarcoplasmic release is insufficient to cause maximal contractile force ( heart at sub optimal conditions)

