Cardiovascular System Flashcards
What is the mediastinum?
Central compartment of thoracic cavity
Surrounded by loose connective tissue
Upper part= vessels to head and neck and limbs
Lower part= anterior, middle, posterior, structures traversing down to abdomen
What is the pericardium?
Membrane (fibroserous sac) enclosing the heart
2 layers= fibrous and serous
Serous has 2 parts (parietal lines fibrous, visceral lines heart)
Why does the serous layer of the pericardium have 2 parts?
Double layer
Lubricating fluid-> mobility
What great vessels enter/leave the RA, RV, LA and LV?
5 great vessels (INTO ATRIA, OUT OF VENTRICLES)
RA= superior and inferior vena cava (return deoxy blood from body circulation into RA) RV= pulmonary artery (splits into L and R, carries deoxy blood from RV to lungs)
LA= pulmonary veins (splits into L and R, carries oxy blood from lungs into LA) LV= aorta (carries oxy blood from LV to systemic circulation)
What are the branches off the aortic arch?
Aortic arch is between ascending and descending aorta (travels backwards)
BRACHIOCEPHALIC TRUNK
Right subclavian artery
Right common carotid artery
LEFT COMMON CAROTID ARTERY
LEFT SUBCLAVIAN ARTERY
What are the subclavian arteries?
Paired major arteries of the upper thorax below the clavicle
Arteries supplies limb (receives blood from aortic arch)
(Vein drains limb)
What are the carotid arteries?
Blood vessels that carry oxygen-rich blood to the head, brain and face
What kind of autonomic control is the vagus nerve under?
Parasympathetic
What are the brachiocephalic arteries?
First branch of the aorta
Supplies blood to tissues of the brain and head (and R arm)
R common carotid
R subclavian
What are the brachiocephalic veins?
Innominate vein
Returns oxygen-depleted blood from upper limbs, neck and head (to heart)
What are the main valves in the heart and where are they/
ATRIOVENTRICULAR VALVES
Mitral (bicuspid)
Tricuspid
SEMILUNAR VALVES (in arteries leaving the heart
Aortic
Pulmonary
What order are the heart valves reached in circulation?
Tricuspid
Pulmonary
Mitral
Aortic
What is the tricuspid valve?
Closes off RA that holds blood coming in from body
Allows blood to flow from RA to RV
Prevents backflow of blood from RV to RA when blood is pumped out of RV
Connected to the papillary muscles but the Chordae tendineae (prevents prolapse or inversion into RA)
What is the pulmonary valve?
Closes off RV
Opens to allow blood to be pumped from the heart to lungs (via pulmonary artery) to receive oxygen
What is the mitral valve?
Closes off LA that collects oxygen-rich blood from lungs
Allows blood to pass from LA to LV
Prevents backflow of blood from LV to LA when blood is pumped out of LV
Anterior cusp
Posterior cusp
What is the aortic valve?
Closes of LV
Opens to allow blood to leave the heart to the body (via aorta)
What cusps are in the tricuspid valve?
Anterior cusp
Septal cusp
Posterior cusp
What cusps are in the pulmonary valve?
Anterior semilunar cusp
Right semilunar cusp
Left semilunar cusp
What are the superior and inferior vena cava?
Bring deoxygenated blood from body to heart
SUPERIOR= from head and upper body-> into RA of heart INFERIOR= from lower body-> into RA of heart
How does blood return from the head and neck to the heart and then back to head?
Blood from head-> enters RA (via superior vena cava)
Blood flows through tricuspid valve into RV
RV pumps blood to lungs (where it absorbs O2) via pulmonary valve
Oxygen-rich blood returns from lungs-> enters LA
Blood flows through mitral valve into LV
LV contract-> blood pumped through aortic valve into aorta
Aorta-> common carotid arteries-> head
What arteries supply oxygen-rich blood to the heart tissue?
Coronary arteries
What veins remove deoxygenated blood from the heart tissue?
Cardiac veins
Describe coronary circulation
Circulation of blood in blood vessels of the heart muscle
Coronary arteries
Cardiac veins
What type of heart damage is the most common cause of UK death?
Damage to coronary arteries
Atheroma and atherosclerosis or MI
What are the coronary arteries?
RIGHT CORONARY ARTERY
Sino-atrial nodal branch of RCA
Right marginal branch of RCA
Posterior interventricular branch of RCA
LEFT CORONARY ARTERY
Circumflex branch of LCA
Left marginal branch of circumflex branch
Anterior interventricular branch of LCA
Diagonal branch of anterior interventricular branch
What are the cardiac veins?
Great cardiac vein
Small cardiac vein
Posterior cardiac vein
Middle cardiac vein
Right marginal vein
Anterior veins of RV
NB. Coronary sinus is where veins come off
What is the cardiac conduction system?
Group of specialised cardiac muscle cells in heart walls that signal to heart muscle causing it to contract
Specialised means the heart independently generates and propagates electrical activity (can beat even without its nerve supply)
Extrinsic nerve supply from ANS to modify and control the intrinsic beating
What are the major components of the cardiac conduction system and what happens to them?
- SAN
- Inter-nodal fibre bundles
- AV node
Ventricular bundles (bundle branches and purkinje fibres)
SA node-> anterior/middle/posterior intermodal tracts-> AV node
AV node-> Bundle of His (into right and left bundle branches)
-> Purkinje fibres in ventricular walls
NB. SA nodes also-> Bachmann’s bundle (LA)
How is calcium involved in contraction of the heart?
Electrical event-> calcium transient-> contractile event
Excitation-contraction coupling
What are T-tubules?
Finger-like invaginations from the cell sruface
Carry surface depolarisation deep into the cell
T tubule lies alongside each Z line of every myofibril (spaced approx 2 um apart)
Outline excitation-contraction coupling (on excitation)
Depolarisation-> influx of Ca into myocyte (via L-type Ca channels)
Ca binds to IC SR-Ca release channels-> conformational change
CICR (Ca induced Ca release) from SR
Ca release-> myocyte contraction
Outline excitation-contraction coupling (on relaxation)
Intracellular Ca taken up into the SR by Ca-ATPase (SERCA)
Ca also removed from myocyte by Na/Ca exchanger
Na/Ca exchanger uses the energy gradient from Na to expel Ca into EC matrix
How can the contraction force be described (graphically)?
Sigmoidal relationship
Between log of cytoplasmic Ca concentration and % of maximum force produced
What is the difference in length-tension relationships for cardiac and skeletal muscle?
Cardiac muscle more resistant to stretch
Less compliant than skeletal muscle
Due to properties of the extracellular matrix and cytoskeleton
Only ascending limb of the relation important for cardiac muscle
What are the two types of contraction?
Isometric (muscle fibres don’t change length, pressures in both ventricles increase)
Isotonic (shortening of fibres and blood is ejected from ventricles)
Define: preload
Weight that stretches muscle before it’s stimulated to contract
Define: afterload
Weight not apparent to muscle in resting state
Only encountered when muscle has started to contract
What is the relationship between afterload and shortening/shortening velocity?
In isotonic contraction
Inverse linear relationship between afterload and shortening
Almost inverse linear relationship between afterload and shortening velocity
What happens if preload increases?
There is an initial enhanced stretch which-> increased ability of the muscle to produce more force (shifts the graph to the right)
I.e. a greater afterload will result in more shortening than before
What are the in-vivo correlates of preload?
As blood fills the ventricles during the relaxation phase (or diastole) of the cardiac cycle it stretches the resting ventricular walls
Stretch or filling determines the preload on the ventricles before ejection
Preload is dependent upon venous return to the heart
Exercise increases pre-load
What are the in-vivo correlates of afterload?
The load against which LV ejects blood after opening of the aortic valve
Any increase in afterload decreases the amount of isotonic shortening that occurs and decreases the velocity of shortening
I.e. small ventricular filling leads to a smaller contraction as the ventricular cardiac muscle responds less effectively to the afterload of the arterial blood pressure
What are the measures of preload?
End-diastolic volume
End diastolic pressure
Right atrial pressure
What is the simple measure of afterload?
Diastolic arterial blood pressure
How can heart contraction be altered?
INTRINSIC MECHANISMS
Frank-Starling relationship
Rate-induced regulation
EXTRINSIC MECHANISMS
Autonomic NS
Endocrine system
Blood gases and pH
What is the Frank-Starling relationship?
Increased diastolic fibre length increases ventricular contraction
Consequence: ventricles pump greater stroke volume so, at equilibrium, cardiac output exactly balances the augmented venous return
What 2 factors is the F-S relationship due to?
Changes in number of myofilament cross bridges that interact
Changes in Ca sensitivity of the myofilaments
Why do changes in number of myofilament cross bridges that interact affect the F-S relationship?
At optimum sarcomere length, there is maximum interdigitation between thick and thin filaments
At shorter lengths than optimal, actin filaments overlap on themselves-> reducing no. of myosin cross bridges that can be made
Why do changes in Ca sensitivity of the myofilaments affect the F-S relationship?
Ca sensitivity changes with changes in sarcomere length
At longer sarcomere lengths, the affinity of Troponin C for Ca is increased
-> less Ca required for the same amount of force produced
OR
With stretch the spacing between myosin and actin filaments (“lattice spacing”) decreases
With decreasing myofilament lattice spacing, the probability of forming strong binding cross- bridges increases
This produces more force for same amount of activating calcium
What is stroke work?
Work done by the heart to eject blood under pressure into the aorta and pulmonary artery
What is stroke volume?
Volume of blood ejected during each stroke by each ventricle
Affected by afterload, preload and contractility
What is pressure (P) in the stroke work equation?
Pressure at which blood is ejected
Greatly influenced by structure
What is the formula for stroke work?
Stroke work= SV x P
What is the Law of Laplace (concept)?
Law states that: when the pressure within a cylinder is held constant, the tension on its walls increases with increasing radius
Therefore, if pressure and tension (wall stress) remain constant, wall thickness must be increased or radius of the cylinder must be decreased
What is the Law of Laplace (formula)?
T = (PR)/h
T= wall tension P= internal pressure R= cylindrical radium h= height/length of cylinder
Why is the Law of Laplace important physiologically?
Radius of curvature of walls of LV is less than that of RV allowing LV to generate higher pressures with similar wall stress (to combat the higher aortic blood pressure than pulmonary BP)
Facilitates late ejection
Wall stress kept low in giraffe by long, narrow, thick-walled ventricle
In frog, where pressures are low the ventricle is almost spherical
Failing hearts often become dilated which decreases pressure generation and ejection of blood and increases wall stress by increasing the radius
Outline the cardiac cycle from atrial systole
DIASTOLE
D3. Late (slow filling)
D4. Atrial systole
SYSTOLE
S1. Isovolumetric ventricular contraction
S2. Ventricular ejection (rapid, reduced)
DIASTOLE
D1. Isovolumetric ventricular relaxation
D2. Late (rapid filling)
What is diastole?
Ventricular relaxation during which ventricles fill with blood
4 sub-phases
What is systole?
Ventricular contraction when blood is pumped into the arteries
2 sub-phases
How can you calculate stroke volume with systolic and diastolic volumes?
End diastolic volume - end systolic volume = stroke volume
What is the ejection fraction and what is the formula to calculate it?
EF = SV/EDV
Percentage of EDV ejected
At peak exercise >80%
In heart failure
What happens in atrial systole? Mechanical events Changes in pressure and volume Electrocardiogram Heart sounds
MECHANICAL EVENTS
Just before, blood flows passively through AV valves (tricuspid and mitral)
Atrial depolarisation-> atrial contraction-> tops up volume of blood in ventricles
CHANGES IN PRESSURE AND VOLUME
As atria contract, ‘a wave’ can be seen (due to increased atrial pressure)
Blood also pushed back into jugular vein-> wave in jugular venous pulse
ELECTROCARDIOGRAM
SAN activation-> atrial depolarisation (P wave)
HEART SOUNDS
No heart sound heard (4th maybe as an abnormality in congestive heart failure, pulmonary embolism or tricuspid incompetence)
What happens in isovolumetric contraction? Mechanical events Changes in pressure and volume Electrocardiogram Heart sounds
MECHANICAL EVENTS
Occurs just as ventricles depolarise
Interval between AV valve closing and semi-lunar valves (aortic/pulmonary) opening
CHANGES IN PRESSURE AND VOLUME
AV valves close as ventricular pressure exceeds the atrial pressure
Since the AV and SL valves are closed-> no blood movement out of ventricles, just increased pressure (approaching aortic pressure)
ELECTROCARDIOGRAM
Ventricular depolarisation marked by QRS complex
HEART SOUNDS
LUB (of lub-dub) due to AV valves closing and associated vibrations
What happens in rapid ejection? Mechanical events Changes in pressure and volume Electrocardiogram Heart sounds
MECHANICAL EVENTS
Ventricular muscle walls undergo isotonic contraction-> push blood out ventricles
SL valves open
CHANGES IN PRESSURE AND VOLUME
As ventricles contract, pressure within them exceeds pressure in aorta and pulmonary arteries
When SL valves open-> volume of ventricles decreases
RV contraction pushes tricuspid valve slightly into atrium (-> small jugular vein wave ‘c wave’)
ELECTROCARDIOGRAM
No changes
HEART SOUNDS
No heart sounds
What happens in reduced ejection? Mechanical events Changes in pressure and volume Electrocardiogram Heart sounds
MECHANICAL EVENTS
Marks end of ventricular systole
Aortic and pulmonary (SL) valves begin to close
CHANGES IN PRESSURE AND VOLUME
Blood flow from ventricles decreases-> ventricular volume decreases more slowly
Pressure in ventricles falls below that in arteries so blood begins to flow back-> SL vales close
ELECTROCARDIOGRAM
Ventricular repolarisation marked by T wave
HEART SOUNDS
No heart sounds
What happens in isovolumetric relaxation? Mechanical events Changes in pressure and volume Electrocardiogram Heart sounds
MECHANICAL EVENTS Beginning of diastole Aortic and pulmonary valves (SL) shut completely AV valves remain closed Atria fill with blood
CHANGES IN PRESSURE AND VOLUME
Atrial pressure rises as blood volume increases
Blood pushing on tricuspid valve gives a second jugular pulse (‘v wave’)
Aortic valve shuts-> rebound pressure wave against the valve (distended aortic wall relaxes)
Recoil reduces the aortic pressure (seen as dichrotic notch)
ELECTROCARDIOGRAM
No changes
HEART SOUNDS 2nd sound (DUB) when aortic and pulmonary valves close
What happens in rapid ventricular filling (late diastole)? Mechanical events Changes in pressure and volume Electrocardiogram Heart sounds
MECHANICAL EVENTS
AV valves open and blood flows rapidly (passively) into ventricles
CHANGES IN PRESSURE AND VOLUME
Ventricular volume increases as atrial pressure falls
ELECTROCARDIOGRAM
No changes
HEART SOUNDS
3rd (abnormal)= can signify turbulent ventricular filling due to sever hypertension or mitral incompetence
What happens in reduced ventricular filling (late diastole)? Mechanical events Changes in pressure and volume Electrocardiogram Heart sounds
MECHANICAL EVENTS
Diastasis
Ventricles fill more slowly as pressure difference between atria and ventricles decreases
CHANGES IN PRESSURE AND VOLUME
Ventricular volume increases more slows
ELECTROCARDIOGRAM
No changes
HEART SOUNDS
No heart sounds
What are the a, c and v waves (in atrial pressure)?
A WAVE (in atrial systole) As atria contract, 'a wave' can be seen (due to increased atrial pressure) Blood also pushed back into jugular vein-> wave in jugular venous pulse
C WAVE (in rapid ejection) RV contraction pushes tricuspid valve slightly into atrium (-> small jugular vein wave 'c wave')
V WAVE (in isovolumetric relaxation)
Blood pushing on tricuspid valve gives a second jugular pulse ('v wave')
What happens on an ECG?
P= Atrial depolarisation QRS= Ventricular depolarisation T= Ventricular repolarisation
When are heart sounds made?
4th (abnormal)
1st (LUB)= AV valves close and associated vibrations
2nd (DUB)= SL valves close
3rd (abnormal)= can signify turbulent ventricular filling due to sever hypertension or mitral incompetence
On a graph showing changes in pressure and volume, what does it mean when pressure lines cross (i.e. atrial and ventricular pressure or ventricular and aortic pressure)?
Valves closing
What is seen as a dichrotic notch in aortic pressure?
Aortic valve shuts-> rebound pressure wave against the valve (distended aortic wall relaxes)
Recoil reduces the aortic pressure
What does the Wiggers diagram show?
RIGHT HEART PRESSURE
Pulmonary artery pressure
Right ventricular pressure
LEFT HEART PRESSURE
Aortic pressure
Left arterial pressure
VENTRICULAR VOLUME
Including EDV and ESV
HEART SOUNDS
S3, S1, S2, S3, S1
MITRAL VALVE
O or C
AORTIC VALVE
O or C
ECG
TIME (sec)
At the top of the Wiggers diagram, the stages of contraction are…
Atrial systole Isovolumetric contraction Ejection (rapid then reduced) Isovolumetric relaxation Rapid filling Reduced filling (diastasis)
What happens to pressures in pulmonary circulation?
Patterns essentially identical in L and R heart but pressures in R heart are much lower
Both ventricles eject same amount of blood
What pressure is in the RA, RV, pulmonary artery, LA, LV, aorta?
Pressure (mmHg)
RIGHT SIDE
RA= 0-8
RV= 25/5
Pulmonary artery= 25/12
LEFT SIDE
LA= 8-10
LV= 125/5
Aorta= 120/80
What is the pulmonary artery wedge pressure (PAWP) and what can elevation indicate?
4-13mmHg
Taken from a branch of pulmonary artery when the back pressure has been occluded
Elevation can indicate LV failure, mitral insufficiency, mitral stenosis
Describe the pressure-volume loop
SEE GRAPH
Volume on x axis
Pressure on y axis
4 sided shape (BL= 4, TL=3, TR= 2, BR= 1)
High volume, low pressure= preload (determined by blood filling the ventricle during diastole)
High volume, high pressure= afterload (represented by blood pressures in aorta and pulmonary artery)
On the pressure-volume loop graph, what happens at X1 (bottom right)?
End diastolic volume, i.e. the preload after max ventricular filling
Blood filling the ventricle during diastole determines the preload that stretches the resting ventricle
On the pressure-volume loop graph, what happens at X2 (top right)?
BPs encountered in great vessels (aorta and pulmonary artery) represent the afterload
On the pressure-volume loop graph, what happens between X2 and X3 (top right-> left)?
Between X2 and X3, isotonic contraction of the ventricles occurs
How does the pressure-volume loop relate to the F-S relationship?
The pressure-volume loop can be fitted into the Frank Starling graph
The straight line of the active force is equal to the end-systolic pressure line
What happens to the pressure-volume loop if you increase preload or afterload?
Increasing preload increases stroke volume (increasing X1 increases width of loop)
Increased afterload decreases SV
There is a greater pressure to overcome in order to open the aortic valve, therefore X2 increases and less shortening occurs
What is the contractile capability of the heart?
Simple measure of cardiac contractility is ejection fraction
Contractility is increased by sympathetic stimulation-> Beta-adrenoreceptor activation-> increase cyclic AMP-> phosphorylation of key Ca2+ handling proteins-> Ca2+ channels open for longer-> Ca influx increased-> increased Ca2+ in cytoplasm-> increased force of contraction
During exercise
- Contractility is increased due to increased sympathetic activity
- End diastolic volume is increased due to changes in the peripheral circulation (venoconstriction and muscle pump)
Increasing contractility increases pressure and volume
Decreasing contractility decreases volume and pressure
How long does systole take?
0.3sec
How long does the entire cardiac cycle take?
0.8sec
What is the average heart rate?
72 beats per minute
What is cardiac output?
Amount of blood ejected by each ventricle in one minute
What is the formula for CO and what is a typical value?
CO = HR x SV
CO= 72bpm x 70ml/beat = 5.04L/min
How can you calculate the equilibrium potential?
Nernst equation
What helps maintain the potassium concentration?
Na/K ATPase
What formula can be used to calculate resting membrane potential?
Goldman-Hodgkin-Katz
Takes into account relative permeabilities of ions
What is the duration of a cardiac AP compared to a nerve?
Cardiac action potential is long (several hundred milliseconds)
Duration of AP controls the duration of contraction of the heart
Long, slow contraction is required to produce an effective pump
At rest, membrane potential determined by K
What is a major difference in re-excitability between skeletal and cardiac muscle?
In skeletal muscle repolarization occurs very early in the contraction phase making re-stimulation and summation of contraction possible (can-> tetanus)
In cardiac muscle it is not possible to re-excite the muscle until the process of contraction is well underway hence cardiac muscle cannot be tetanized
Describe the graph of the cardiac AP
Steep vertical AP
Plateau
Gradual decline
Define: absolute refractory period
Time during which no AP can be initiated regardless of stimulus intensity
Relates to Na channel inactivation (Na channels recover from inactivation when the membrane is repolarized)
Define: relative refractory period
Period after absolute refractory where an AP can be initiated but only with stimulus larger than normal
What is full recovery time (regarding refractory period)
The time at which a normal AP can be elicited with normal stimulus
What are the phases of the cardiac AP?
0= upstroke (Na) 1= early repolarisation 2= plateau (Ca) 3= repolarisation (K) 4= resting membrane potential (diastole)
Describe what happens in the plateau phase of a cardiac AP
Calcium influx during early plateau-> trigger Ca release from IC stores
Required for contraction
Activates rapidly (within ms)
What calcium channel antagonists inhibit calcium channel (e.g. in plateau)?
Nifedipine
Nitrendipine
Nisoldipine
Describe what happens during repolarization in a cardiac AP
Gradual activation of K currents
Large K current that is inactive during plateau opens when cells have partially repolarised
What is IK1?
Current responsible for fully repolarising the cell
Large
Flows during diastole
Stabilizes the RMP-> reduced risk of arrhythmias by requiring a large stimulus to excite the cells
Why do different parts of the heart have different AP shapes?
Due to different ionic currently flowing
Different degrees of expression of ionic channels
NB. SAN (more like skeletal AP but with bigger hyperpolarisation) and ventricular (typical cardiac graph)
What is the role of the SAN in initiating the electrical activity of the heart?
Most channels exist in SA node– to some extent
Exception is IK1 – no IK1 in SA node
Very little Na influx – upstroke produced by Ca influx in SAN
Also T-type Ca channels that activate at more –ve potentials than L-type
Ito is very small
Pacemaker current (If) present
What is the natural rhythm of pacemaker cells?
Approx 80 APs (and hence heartbeats) per minute
What is the approximate resting potential of pacemaker cells?
-65mV (but unstable therefore-> more negative)
What is the pre-potential caused by?
Special inward Na+ current into pacemaker cells, along with a decrease in the membrane permeability to K+
I.e. increased Na+ influx, decreased K+ efflux
What influence does the sympathetic nervous system e.g. adrenaline have on pacemaker cells?
Increases Na influx
Seen by increase in pre-potential slope (therefore threshold is reached more rapidly, HR decreased)
What influence does the para sympathetic nervous system e.g. acetylcholine have on pacemaker cells?
Reduces Na influx
Seen by decrease in pre-potential slope ((therefore threshold is reached more slowly, HR increased)
What is the sino-atrial node?
Pacemaker of the heart
A small mass of specialised cardiac muscle situated in the superior aspect of the right atrium
Located in the anterolateral margin between the orifice of the superior vena cava and the atrium
Automatic self-excitation: it initiates each beat of the heart
Since the fibres of the SA node fuse with the surrounding atrial muscle fibres, AP generated in the nodal tissue spreads throughout both atria
At what speed does an AP generated in the nodal tissue spread throughout both atria?
0.3m/s
Produces atrial contraction
Where are inter-nodal fibre fibres and what does it do?
Interspersed among the atrial muscle fibres
Conduct the AP to the AVN with greater velocity than ordinary muscle (1m/s)
Where is the AVN and what does it do?
Located at the border of the RA near the lower part of the interatrial septum
Electrically connects the conduction system between atrial and ventricular chambers.
Produces short delay (approx 0.1s) in transmission
-> Delays fibres in AVN and special junctional fibres that connect the node with ordinary atrial fibres
Why does the AV node produce a short delay?
Allows atria to complete their contraction and empty their blood into the ventricles before the ventricles contract
What is the role of the bundle of His and bundle branches?
As the AV bundle leaves the AV node, it descends in the interventricular septum for a short distance (Bundle of His) and then divides into the right and left bundle branches
These comprise of specialised muscle fibres called Purkinje fibres which terminate in a finger-like fashion on the working myocardial cells
They are very large; conduct the AP at about 6x the velocity of ordinary cardiac muscle (1.5 to 4.0m/s)
What is the role of the Purkinje fibres?
The terminal Purkinje fibres extend beneath the endocardium and penetrate approximately one-third of the distance into the myocardium
They end on ordinary cardiac muscle within the ventricles, and the impulse proceeds through the ventricular muscle at about 0.3 to 0.5 meters per second.
The excitation of the ventricles proceeds upward from the apex of the heart toward its base
What determines the extend of spread of current (in impulse propagation)?
The propagation of AP is due to a combination of passive spread of current and existence of a threshold
Coupling resistance of the cells (gap junction resistance) determines extent of spread of current
What is the purpose of gap junctions in conduction?
Intercellular communication and impulse conduction rely on gap junctions which form at intercalated discs
Describe what deflections are the basis of the ECG
The effects of a wave of depolarisation are detected as the potential difference between two electrodes
When a wave of depolarisation is moving TOWARDS the positive electrode it causes an UPWARD deflection
When a wave of depolarisation is moving AWAY from the positive electrode it causes a DOWNWARD deflection
When a wave of repolarising current is moving TOWARD the positive electrode it causes an DOWNWARD deflection
When a wave of repolarising current is moving AWAY the positive electrode it causes an UPWARD deflection
*Repolarising current is of opposite polarity to depolarising current
If the position of an ECG electrode relative to the heart is known, what can be predicted/
The waveform that it should record assuming a normal process of excitation
Describe chest lead configuration
Use Angle of Louis to find 2nd intercostal space
V1= where the 4th intercostal space meets the sternum (on R)
V2= where the 4th intercostal space meets the sternum (on L)
V4= at the mid-clavicular line in the 5th intercostal space
V3= between V2 and V4
V5= at the anterior axillary line in the 5th intercostal space (immediately below the beginning of the axilla, or under-arm area)
V6= at the mid axillary line in the 5th intercostal space (below the centre point of the axilla)
Where is the neutral ‘zero reference ‘ wire connected?
Right foot/leg= zero reference point
Point of comparison so potentials can be generated
Also removes effect of background electrical noise
Describe limb lead configuration
aVR= R arm aVL= L arm N= R foot aVF= R foot
What cardiac conditions can be detected with an ECG?
Tachyarrhythmias Bradyarrhythmias Myocardial infarction Myocardial ischaemia Cardiomyopathy Assessment of pacing Electrolyte disturbances
What is Einthoven’s triangle?
Equilateral between L arm, L foot and R arm
LEAD 1= R to L arm (L arm considered to be the +ve electrode)
LEAD 2= R arm to L foot (L foot considered to be the +ve electrode)
LEAD 3= L arm to R foot (L foot considered to be the +ve electrode)
What degree are leads 1, 2, and 3 considered to be at?
1= 0 2= +60 3= +120
I.e. The positive pole of Lead 2 is considered to be +60° to the positive pole of Lead I
The positive pole of Lead 3 is considered to be +120° to the positive pole of Lead I
What does it mean if Lead aV is an augmented vector?
Lead aV couples with standard limb leads to form augmented vectors
Describe the 3 augmented leads
aV-R: R arm is considered the positive electrode, and the negative electrode is considered to be half way between the L arm and L foot +ve 0
aV-L: L arm is considered the positive electrode, and the negative electrode is considered to be half way between the R arm and R foot
aV-F: L foot is considered the positive electrode, and the negative electrode is considered to be half way between the R and L arm
What are the standard limb leads and the augmented leads?
Standard= Leads 1, 2 and 3
Augmented= aVR, aVL and aVF
What will the readings of augmented leads be compared to standard limb lead readings?
Bigger
Because they are coupled
Considering Einthoven’s triangle, what are the augmented vectors?
Lead 1 is 0
aV-R is at -150° (150° above the 0° line)
aV-L is at -30° (30° above the 0° line)
aV-F is at +90° (90° below the 0° line, i.e. perpendicular)
How do you achieve a hexagonal reference system?
6 limb leads combined (standard and augmented)
Arranged in 3 pairs of 2 leads which are at right angles to each other:
- Lead I and aVF
- Lead II and aVL
- Lead III and aVR
Are standard or augmented limb leads bipolar?
Standard (limb leads)= bipolar
Augmented (limb leads) and V1-V6 (precordial leads)= unipolar
In leads 1 and 2, are P and QRS positive or negative?
Positive
ECG graph paper has big and small squares, what do they mean?
1 SMALL
1mmx1mm block
Represents 40ms time and 0.1mV amplitude
1 LARGE
5mmx5mm block
Represents 0.2s (200ms) time and 0.5mV amplitude
NB. Amplitude= y
Time= x
What deflection is caused when a wave of depolarisation is moving towards the positive electrode?
Upward (shown by positive waveform)
What deflection is caused when a wave of depolarisation is moving towards the negative electrode?
Downward (shown by negative waveform)
What is the mean vector of wave depolarisation in the ventricles?
Towards the apex of the L ventricle
May be along axis of lead 1 (i.e. at 0 degrees) OR in the direction of aVF (i.e. at +90 degrees)
What is the MFPA?
Mean frontal plane axis of the ventricles
When the waveform is positive (upward deflection), what does this mean about the direction of the wave of depolarisation and the MFPA?
The wave of depolarisation is towards the positive electrode of the MFPA
When the waveform is negative (downward deflection), what does this mean about the direction of the wave of depolarisation and the MFPA?
The wave of depolarisation is away from the positive electrode of the MFPA
Why do waveforms vary in size?
If lead is exactly on MFPA, the signal will be max size (i.e. the angle between the lead and MFPA is 0, and cos0 = 1 = max)
The fraction of the max signal obtained in each lead can be calculated using SOH CAH TO A (if right angled triangles are drawn)
Why are equipotential and negative waves measured?
The value of cos90= 0
Hence the value of (MPFA cos90) is also zero
This explains why a lead with its axis at right angles to the MFPA show no signal (or a small equipotential)
Cosines of angles between 90 and 270 are negative
Thus when a lead is more than 90 to MFPA the ECG will show downward (negative) rather than upward deflections
What is the range of MFPA?
Normal range of the MFPA is between -30° and +90°, and may vary between patients
This depends on the orientation of the heart in the chest
If a patient has an MFPA that is more negative than -30°, they are exhibiting left axis deviation (enlarged left ventricle e.g. aortic stenosis)
If a patient has an MFPA that is more positive than +90°, they are exhibiting right axis deviation (enlarged right ventricle which could be pulmonary disease)
How do you calculate the QRS axis?
Summation of vectors
EXAMPLE 1 QRS axis = Lead 1 + aVF If lead 1= +8 and aVF= +3 Tan(x) = 3/8 x = 21 degrees QRS axis = 21 degrees
EXAMPLE 2 If lead 1= +12 and aVF= -14 Tan(x) = 14/12 x= 49 degrees QRS axis = -49 degrees Left axis deviation (more negative than -30)
EXAMPLE 3 If lead 1= -3 and aVF= 8 Tan(x) = 3/8 x= 21 degrees QRS axis = +111 degrees Right axis deviation (more positive than +90)
Describe how chest (pre-cordial) lead recordings are obtained
6 unipolar leads
Designation as V1 – V6
All electrodes are positive
I.e. for each lead, chest lead is a positive pole
Septum depolarisation occurs first, and is from left to right
MFPA is then in the right to left direction
How is the QRS complex shown by pre-cordial leads?
V6 records small wave of depolarisation AWAY from the electrode, then large wave TOWARDS (qR wave)
V1 records a small wave of depolarisation TOWARDS the electrode, then a large wave AWAY (rS wave seen in diagram)
These combine to form the QRS complex seen on an ECG
V3 records a biphasic (both direction) wave known as the transition zone
The ECG then combines the recordings at the 6 chest electrodes, with the hexagonal reference system for the 6 leads (standard + augmented)
What is the duration and amplitude of the P wave, PR interval, QRS complex, Q wave and QT interval?
P wave= duration
What is normal heart rate?
60-100bpm
How is heart rate calculated from an ECG?
Count number of squares between each QRS complex and divide 300 by this number
Count number of QRS complexes in 10 seconds, and multiply this number by 6
What does the PR interval represent?
Time taken for wave of depolarisation to migrate from one side of the AVN to the other
The AVN acts like a safety valve to separate atrial and ventricular systole
What are the steps for ECG?
- Is it the correct recording?
- Identify the leads
- Check the calibration and speed of the paper (25 mm/s, 1mV = 10mm)
- Identify the rhythm
- Look at the QRS axis
- Look at the P wave
- Look at the PR interval
- Look at the QRS complex
- Determine the position of the ST segment
- Calculate the QT interval
- Look at the T wave
- Check!
What are common abnormalities of cardiac rhythm that can be picked up on the ECG?
Sinus tachycardia Atrial fibrillation Atrial flutter AV nodal reentrant tachycardia (AVNRT/AVRT) Pre-excitation syndrome Heart block Bundle branch block (Right BBB and left BBB) Ventricular tachycardia (monomorphic) Ventricular fibrillation
What abnormalities are seen in sinus tachycardia? Heart rate Rhythm P wave PR interval QRS in seconds
P waves have normal morphology, towards positive electrode of Lead 2 (RA-> LF, similar to axis of heart) and reverse direction of Lead aVR
HEART RATE
>100 bpm
(Atrial 100-200, ventricular 100-200)
RHYTHM
Regular
P WAVE
Before each QRS, identical (normal)
PR INTERVAL
0.12-0.20s
QRS
What abnormalities are seen in atrial fibrillation? Heart rate Rhythm P wave PR interval QRS in seconds
P waves absent, replaced by oscillating baseline fibrillation waves
HEART RATE
Atrial rate= 350-600bpm (all atrial myocytes are firing rapidly, not completely efficient therefore blood pools in the atria-> compromised CO and increased stroke risk)
Ventricular rate= 100-180bpm (irregular rhythm due to atria irregularity, ventricles rapidly depolarise-> narrow QRS complex)
RHYTHM
Irregular
P WAVE
Fibrillatory (fine to course)
PR INTERVAL
n/a
QRS
What abnormalities are seen in AVN reentrant tachycardia? Heart rate Rhythm P wave QRS in seconds
Narrow complex tachycardia
Common in teenagers
Re-entrat circuit within AV node
HEART RATE
Atria and ventricles contract at same time
RHYTHM
Regular or variable
P WAVE
Often buried within QRS or just after QRS
QRS
Regular
What abnormalities are seen in pre-excitation syndrome? P wave PR interval QRS in seconds Characteristics
Accessory pathway (connect atrium to ventricle, which is an abnormal physical pathway)
- 1/3= conduct antegradely (WPW)
- 2/3= conduct retrogradely (concealed pathways)
Depolarisation of the ventricles early (pre-excitation)
- > slurring of the QRS complex and lack of regulation by the AVN
- > electrical activity conducted faster
- > increased HR
P WAVE
Before each QRS, identical (normal)
PR INTERVAL
10s
CHARACTERISTICS
Delta wave distorts QRS
Predisposes to accessory pathway tachycardias (AVRT)
What is a heart block?
AV nodal block
1st degree (prolonged PR interval >20s) 2nd degree (Mobitz type 1 or 2) 3rd degree (complete heart block)
Describe the 2 types of 2nd degree heart blocks
MOBITZ TYPE 1 (Wenckebach)
Disease of AV node
Progressive lengthening of PR interval followed by a blocked P wave (no QRS)
Then PR interval resets and cycle repeats
MOBITZ TYPE 2
Disease of His-Purkinje conduction system
Intermittently non-conducted P waves not preceded by PR interval lengthening and not following by PR interval shortening
Describe 3rd degree heart blocks
Complete Heart Block
1st rhythm= P waves with regular P to P interval
2nd rhythm= QRS complexes with a regular R to R interval
No apparent relationship between P waves and QRS complexes
What 2 ECG changes are seen in the bundle branch block?
- QRS complex widens (>0.12s) – when the conduction pathway is blocked, it takes longer for the electrical signal to pass throughout the ventricles
- QRS morphology changes – depends on lead, and R vs. L BBB
What abnormalities are seen in right bundle branch block? P wave PR interval QRS in seconds Characteristics
Normally left bundle branch depolarizes normally but right bundle has a conduction block
Wide QRS complex in leads overlying right ventricle
Seen as RSR complex instead of a QRS complex (like rabbit ears)
P WAVE
Before each QRS, identical
PR INTERVAL
0.12-0.20s
QRS
>0.12
CHARACTERISTICS
RSR in V1
What abnormalities are seen in left bundle branch block? P wave PR interval QRS in seconds Characteristics
Right ventricle depolarises first
Wide QRS complex in leads opposite the left ventricle
P WAVE
Before each QRS, identical
PR INTERVAL
0.12-0.20s
QRS
>0.12
CHARACTERISTICS
RR in V5
What abnormalities are seen in ventricular tachycardia (monomorphic)?
Medical emergency -> won’t normally see ECGs of it
Irregular rapid contraction of the ventricles, not as a result of depolarisation through the normal AVN and rapid conduction system
This leads to a broad QRS complex
Unstable rhythm disturbance; often occurs in the middle/just after MI
May lead to cardiac ischaemia
What abnormalities are seen in ventricular fibrillation? Heart rate Rhythm P wave PR interval QRS in seconds
Most commonly identified arrhythmia in cardiac arrest patients
Ventricular muscle twitches randomly rather than in a coordinated fashion
HEART RATE
300-600bpm
Severe darangement (usually-> death within mins)
RHYTHM
Extremely irregular
P WAVE
Absent
PR INTERVAL
N/a
QRS
Fibrillatory baseline
What is the role of circulation?
To transport blood around the body
To deliver oxygen, nutrients and signalling molecules
To remove CO2 and metabolites
To regulate temperature
How is blood flow achieved?
By action of a muscular pump (heart)
Generates a pressure gradient that propels blood through a network of tubes (blood vessels)
What role do the ventricles have in circulation?
Left and right ventricles are 2 pumps
Physically coupled and pump through the systemic and pulmonary circulations
Why isn’t diffusion sufficient for transport?
Only for movement of materials through tissues
Only effective over short distances so a capillary needs to be 10um from every cell
Highly branched structure necessary
What is the structure of the circulation?
Highly specialised
Consists of different vessel types (distinct structures which are highly appropriate for their function)
Large elastic arteries- act as conduits and dampening vessels
Small muscular arteries
Arterioles- have extensive smooth muscle in their walls so they can regulate their diameter and resistance to blood flow
Capillaries- very numerous and have thin walls to facilitate transport and diffusion
Venules
Medium sized and large veins- highly compliant vessels which act as a reservoir for blood volume
What would happen in the CO from both ventricles was different?
Blood would pool
CO from RV and LV needs to be same despite differences in pressue
What is the difference in relative areas and volumes within each circulatory system?
Relatively equal
What are capillaries primarily related to?
Exchange function
What are veins and venules primarily related to?
Reservoir function
What happens to the diameter and cross section of blood vessels from the aorta to the capillaries?
The diameter of the blood vessels changes dramatically from the aorta (25mm in man) to the capillaries (5um = 0.005mm)
As a result of the change in diameter and the expansion of components of the vascular system due to branching there are large changes in the cross-sectional area of the vasculature at different levels
Billions of capillaries and this segments represents the largest cross-sectional are of the circulation
This presents a huge surface area for exchange to take place
Although the volume in a single capillary is tiny, the equivalent of the whole cardiac output passes through the capillary bed every minute
Where is the majority of blood volume contained?
Within the venous part of the circulation
Regulation of capacitance of the veins and venules regulates how much blood is stored and influences venous return to the heart and ventricular work via the F-S effect in the heart
Why does blood flow?
Due to pressure difference
Resistance important
Describe Hales horse experiment
Very simple model of the circulation
Assumes the action of the heart (pump) has established a pressure in the tank (the aorta) equivalent to 8 ft of water (as measured by Hales) – this is P1
This drives a steady flow (Q) through the circulation
The branching vessels of the circulation are simplified into a single long rigid pipe for the purposes of this model
Pressure drops along this pipe due to viscous losses of energy (friction), so that the pressure measured at the end (P2) is lower than at P1 – this pressure difference drives the flow (Q)
At the end of the circulation the system empties into the right atrium
What is Ohm’s law?
Electrical circuit
V= I x R
V= voltage difference I= current flow R= resistance
What is Darcy’s law?
Fluid circuit
P = Q x R
P= pressure change Q= volumetric flow R= resistance
What is the formula for MBP and what causes it?
MBP = CO x PVR
Relationship is an approximation since flow in the circulation is not steady
Due to intermittent pumping of the heart
Blood vessels are not rigid
How can you estimate the resistance of circulation?
Relationship between pressure and flow
Regulation of flow is achieved by variation in resistance while blood pressure remains relatively constant
What vessels are the most resistant to flow?
Small arteries and arterioles
What is Poiseuille’s equation?
R= (8Ln/πr^4)
Poiseuille’s equation emphasizes the importance of arterial diameter as a determinant of resistance
Relatively small changes in vascular tone (vasoconstriction/ vasodilation) can produce marked changes in flow
HALVING THE RADIUS DECREASES THE FLOW 16 TIMES
What 3 variables determine resistance?
Fluid viscosity (n, eta) -> not fixed but in most physiological conditions is constant
Length of tube/vessel (L)- > fixed- lengths of blood vessels remain constant
Inner radius of tube/vessel (r)-> variable- main determinant of resistance
What is the difference in blood flow distribution to organs at rest and during exercise?
During exercise, don’t need blood flow to kidneys
What kinds of flow occur in vessels?
Laminar flow
Viscosity
Shear rate
What is laminar flow?
The normal circulation flow is laminar, i.e. the fluid behaves as if it flows in layers or streamlines
shear
Laminar flow can be demonstrated by injecting a dye into fluid
What is viscosity?
Dynamic viscosity (µ) is a measure of the resistance of a fluid to deform under shear stress
Resistance arises as a result of the resistance due to friction between fluid laminae moving at different velocities
What is shear rate?
Shear rate = S = dv/dr
u= velocity of blood flow
r= radial dimension
A force per unit area (the pressure difference) is needed to move the fluid in opposition to viscosity
The flow velocity on the surface of the vessel wall is zero (so called no slip condition) but in a flowing fluid, the velocity of each lamina increases progressively as you move further way from the wall
The spatial velocity gradient is called the shear rate (s)
What is the shear stress (τ)?
Shear rate x dynamic viscosity
τ = (dv/dr) x µ
µ= dynamic viscosity
What happens to the velocity of layers as distance from the wall increases?
Velocity of layers increases
What does it mean to have ‘high shear stress’?
High shear stress, as found in laminar flow, promotes:
- Endothelial cell survival and quiescence
- Cell alignment in the direction of flow
- Secretion of substances that promote vasodilation and anticoagulation
What does it mean to have ‘low shear stress’?
Low shear stress, or changing shear stress direction as found in turbulent flow, promotes:
- Endothelial proliferation and apoptosis
- Shape change, and secretion of substances that promote vasoconstriction
- Coagulation, and platelet aggregation
What is the formula for pulse pressure?
PP = SBP - DBP
Pulse pressure = systolic bp - diastolic bp
What is the formula for mean blood pressure?
MBP = DBP + 1/3PP
How are systolic and diastolic pressure recorded?
SBP/DBP (e.g. 110/70)
When does the aortic valve open?
During systole
Due to the difference in pressure between the ventricles and the aorta
What causes the difference in ventricular and aortic pressure in diastole?
When the aortic valve closes
Ventricular pressure falls rapidly BUT aortic pressure only falls slowly in diastole
(Due to elasticity of the aorta and large arteries which buffer change in pulse pressure)
How is arterial compliance related to pulse pressure?
During ejection, blood enters the aorta and other elastic arteries faster than it leaves them
~40% of the stroke volume is stored by the elastic arteries
When the aortic valve closes, ejection ceases but due to recoil of the elastic arteries, pressure falls slowly and there is diastolic flow in the downstream circulation
This damping effect is sometimes termed the “Windkessel”
How much of the stroke volume is stored by the elastic arteries?
40%
What is ‘Windkessel’?
The damping effect
Reduced by age and when arteries become stiffer (decreased arterial compliance)
NB. PP increases
What is circumferential stress?
σ = tension force (T) / wall thickness (h)
Tension force (according to Law of Laplace= P x r)
σ = (P x r) / h
What does maintained high circumferential stress cause?
Vessel distension
