Cardiac Physiology Flashcards
Is cardiac muscle striated muscle? How does its cells microscopic structure compare to skeletal muscle?
Yes
Myofibrils identical to skeletal muscle with same banding and mechanism
Same sarcolemma with t tubules at the z lines, sarcoplasmic reticulum surrounds in similar manner.
Differences between cardiac and skeletal muscle cellular layout
What is the functional implication
Individual cells are tightly coupled mechanically and electrically by branching and interdigitation of the cells and intercalated discs forming membrane junctions.
Functionally means cardiac contraction is all or nothing
What is the term for a single cell containing several nucli
Is cardiac muscle true one
Syncitium
No - though cells all interconnected each cell has a single nucleus and is surrounded by the sarcolemma
AP function of cardiac muscle and difference to skeletal
Allows rapid low resistance conduction of AP along length of cells
Easy transmission between cells through intercalated discs
What are intercalated discs
Gap junctions - open channels connecting cytoplasm of adjacent cells
How does cardiac muscle mitochondria and capillary supply compare with skeletal muscle?
Higher in both
Events in cardiac muscle post initiation of action potential?
Calcium ingress through voltage sensitive Ca channels
Raising calcium causes release of Ca from sarcoplasmic reticulum
Ca binds to trop C and results in movement of tropomyosin exposing binding sites on actin
Myosin heads attach and move
Atp binds causing release of head then is hydrolysed to adp and pi resetting the system.
Calcium released and returned to sarcoplasmic reticulum by calcium magnesium ATPase
Types of action potential in cardiac muscle? Tissues associated.
Fast response - contractile myocardial cells and conduction system cells
Slow response - SA and AV nodal cells
What is the term for the spontaneous depolarisation of cardiac pacemaker cells
Automaticity
Phases of a fast response cardiac action potential (overview )
0 - rapid depolarisation
1 - early rapid repolarisation
2 - prolonged plateau
3 - final rapid repolarisation
4 - resting membrane potential
Resting membrane potential of fast response cardiac muscle cells
-90mV
How is the cardiac cell fast response negative membrane potential maintained?
Retention of anions (such as proteins, sulphites, phosphates) in cell but facilitation of cations to leave (permeable to K which diffuses down concentration gradient to leave cell until equilibrium reached between the concentration gradient and electrostatic attraction then Na/KATPase pumps return K and exchange Na out).
What is the Nernst equation?
E = (RT/FZ) x log10 ([Ke]/[Ki])
Membrane potential = (gas constant x absolute temp)/(fariday constant x valency) x log10 (external concentration/internal concentration)
Can be dervived to
E = 62/z x log10 ([Ke]/[Ki])
Given internal concentration of K is 150 and external is 5 what is the membrane potential it exerts over the membrane of a cardiac muscle cell
E = 62/1 x log10 (5/150)
= -94
Why is k the main determinant of cardiac muscle cell resting potential?
Permiable to k
Not to Na so leakage of this is small making little difference to the potential (around 4mV move +ve)
How is phase 0 initiated in cardiac fast response action potential
Resting membrane potential increased by electrical stimulus (less negative)
Reaches threshold potential
Fast sodium channels open and potassium channels close
Rapid influx of Na down concentration gradient and towards electrostatic attraction of intracellular anions
Cell interior reaches membrane potential of +20 and sodium channels close
Mechanism of phase 1 of cardiac fast cell action potential
Brief fall in membrane potential from +20 towards 0
Caused by potassium flow out of cell down electrical and chemical gradients
Opening of slow L-type ca channels providing prolonged influx of Ca ions maintaining +ve intracellular charge. Chloride also follows Na back into cell.
Mechanism of stage 2 of cardiac fast action potential
Continued influx of Ca through slow l-type ca channels balancing the efflux of potassium, membrane potential maintained around zero or slightly positive.
Mechanism of stage 3 of fast action cardiac action potential
Rapid increase in potassium permeability
Transmembrane potential restored to -90
Though potential is back to baseline the ionic gradients are not yet reestablished.
Mechanism of stage 4 of fast cardiac action potential
ATPase ion pumps exchange na and k restoring ionic gradients back to resting membrane potential.
How do atrial myocytes differ from ventricular myocytes in their fast action potentials
Shorter plateau phase (phase 2) due to much greater early repolarisation current
What controls excitability of cardiac cells?
How can it be influenced?
The difference between resting membrane potential and threshold potential (bigger difference means less excitable)
Influenced by various factors including catecholamines, beta blockers, local anaesthetics, electrolyte levels.
What is the refractory period of a fast response cardiac action potential
Absolute refractory period - The cell cannot be depolarised again during phase 0,1,2 and early stage 3 regardless of stimulus strength as the sodium and ca channels are inactivated
Relative refractory period - during latter part of stage 3 and early stage 4 a stronger than normal impulse can trigger an early AP
Term for combined absolute and relative refractory period
Effective refractory period
What can trigger depolarisation/automaticity outside of the normal pacemaker system
Injury can trigger spontaneous depolarisation of normal myocytes
Where are pacemaker cells found in the heart?
SA, AV, his-purkinje system,
Latent pacemaker cells in other parts of conduction system that can take over if AV blocked.
Phases of cardiac slow response action potential
4 - restoration of ionic gradients
0 - rapid depolarisation
3 - repolarisaiton
During phase 4 of a slow response cardiac action potential what occurs
No resting potential!
Depolarise spontaneously because of increased membrane permeability to cations allowing Na and Ca to leak into cell counteracting and overcoming slow loss of K
Membrane potential gradually increases from maximum diastolic potential of -60mV to threshold potential of -40mV
Mechanism of phase 0 of slow response cardiac action potentials
How does it compare to phase 0 of rapid response cardiac cells
Rapid depolarisation on reaching threshold potential due to opening of t-type calcium (t for transient) channels and influx of calcium
Slower influx than the rapid sodium influx in rapid response cells so slope of phase 0 less steep, and less overall change due to less negative starting membrane potential.
Mechanism of phase 3 cardiac slow response action potential.
Equivalent to phase 3 in rapid response - influx of K causing repolarisation
The phase 1 is absent and phase 2 is very brief so no plateau
Differences between pacemaker and myocardial cell AP
Less negative phase 4 membrane potential
Less negative threshold potential
Spontaneous depolarisation of phase 4
Less steep slope in phase 0
Absence of phase 1/2 plateau
What ion channels and current are responsible for the pacemaker potential
What can influence this
Leaking sodium channels that open when membrane hyperpolarised
Cause an inward current (If) causing depolarisation
Influenced by autonomic nervous system and various drugs
How can pacemaker discharge rate be altered in myocytes
Altering slope of phase 4 (increased slope discharges faster)
Altering threshold potential
Altering hyperpolarisation potential - if membrane reaches more negative value then will take longer to reach threshold
What drugs cause less negative threshold potential in cardiac pacemaker cells
Quinidine
Procainamide
What effect does high acetylcholine levels have on cardiac slow response pacemaker discharge rate
Hyperpolarisation thus slower to reach threshold potential
Rate of sinoatrial node pacemaker resting rate
60-100/min
Location of SA node
Blood supply
RA posterior wall close to entry of SVC (just below and lateral)
Branch of RCA
What pathways connect SA to AV node
Bachmann, Wenckebach, Thorel (anterior, middle, posterior).
Location of AV node
Blood supply
posterior right atrium near interatrial septum near coronary sinus opening
Usually rca
Length of delay at AV node
Purposes
0.13seconds
Allows atrial activation prior to ventricular activation
Where do the bundle branches run? What does the left bundle divide into?
subendocardially down the septum
Anterior and posterior fascicles
How does action potential and contraction spread through the heart wall
What about repolarisation
From the endocardium spreading outwards and apex to base
Repolarisation spreads from outside in.
Factors influencing QRS amplitude
Myocardial mass
Cardiac axis
Anatomical orientation of heart
Distance from heart to sensing electrode
Typical QT interval
350ms
Bazett’s formula to calculate QTc
QTc = QT/square root R-R
When does ventricular contraction end on an ECG
End of T wave (end of repolarisation)
What is the u wave on the ecg?
Uncertain but maybe slow repolarisation of papillary muscles
What is the cardiac axis of the heart?
What is the rough normal direction
The maximum vector of electrical activity produced during ventricular depolarisation
Down and left
How do ECG leads detect a potential difference
Either between 2 electrodes or 1 electrode and a common point
What are the groupings of ecg leads (views)
Frontal plane leads:
Standard I, II, III
Unipolar limb leads avR, avL, avF
Horizontal plane leads
V1-6
How are the standard limb leads set up and how do they work
Record between 2 active electrodes
Record around the sides of Einthovens triangle
Lead I negative right arm, positive left arm
Lead II negative right arm positive left foot
Lead III negative left arm, positive left foot
Characteristics of normal standard limb lead ecg trace
Very similar - all positive p, qrs and t waves
Characteristics of the unipolar limb leads
Record difference in potential between single limb lead and an indifferent (zero potential) electrode centre of einhovens triangle
Low amplitude signals so need amplification
aVR - upper right unipolar arm electrode to indifferent electrode - usually negative waves
aVL - upper left unipolar arm electrode to indifferent electrode
aVF - left leg unipolar electrode to indifferent electrode
How does the ecg calculate the indifferent electrode for analysis of the unipolar limb leads
Combining the activity of the 2 electrodes that are not active (e.g. for aVF left foot as active and combining left and right arm to make indifferent
Locations of the chest electrodes on ecg
V1 fourth ics right of sternum
V2 fourth ics left of sternum
V3 halfway between v2 and v4
V4 fifth ics midclavicular line
V5 fifth ics anterior axillary line
V6 fifth ics mid axillary line
Normal anatomical orientation of heart
Atria posterior
Ventricles anterior/basal with right ventricle anteriolateral to left
What muscle masses predominate on ecg trace
Interventricular septum and left ventricle free wall
Method to calculate heart rate from ECG
Interval in seconds between r waves and dividing 60 by that number
Number of r waves in a 6 second trace and x10
Usual paper speed and square sizes on ecg
Usually 2.5cm/sec
Thus each large square (5mm) represents 200ms and each small square (1mm) 40ms
Normal range for cardiac axis
0 to 90o
Calculation of cardiac axis from ecg (mathematical and why)
Lead one reads directly left to right (0o)
Lead aVF reads directly top to bottom (90o)
Determine amplitude of qrs in both (subtract hight of s wave from hint of r wave)
Tan(angle ) = amplitude aVF/amplitude I
Angle = tan-1 amplitude aVF/amplitude I
At what angles do leads I, II, III and aVF run at?
0
60
120
90
What are left and right axis deviation
Left axis <0o
Right axis >90o
What leads are typically used interop for ecg monitoring?
Why
sII and V5
II best for p waves
V5 best for monitoring ST changes
In a healthy young person what happens to heart rate with inspiration and expiration
Why
Increases on inspiration
Decreases on expiration
Breath in stretch lungs, vagaries stimulation, inhibits cardio inhibitory centre in medulla stimulating SA node
Causes of sinus Bradycardia
Young and fit
Sleeping
Beta blockers, anaesthetics, digitalis, limiting calcium channel blockers
Myxodeaema
Uraemia
Glaucoma
Increases icp
Causes of sinus tachycardia
Hypovolaemia
Anxiety
Pain
Thyrotoxicosis
Toxaemia
Cardiac failure
Drugs
At what heart rate is ventricular filling impaired?
140
Effect of high and low k on ecg (pathology and signs)
Hyperkalaemia - less negative resting potential closer to threshold - initially more excitable with risk of vt and vf but then reduction in rapid depolarsiation and loss of plateau giving poor contraction. When rmp comes close to tp heart stops in ventricular diastole.
Short qt, narrow peaked ts, widened qrs, pr prolongation then loss of p waves, then sine wave.
Hypokalaemia - more negative rmp, less excitable heart but increased automaticity
Prolonged pr, flat t wave, u wave, qt prolonged, progressing to twi and st depression
Effect of high and low calcium on ecg
Low calcium - flat prolonged st segment and qt interval, risk of pvcs and vt
High calcium - makes tp less negative, decreases conduction velocity and shortens refractory period. In very high concentrations can cause calcium rigor . Produces prolonged pr, wide qrs, short qt, broad t.
Effects of hypomagnesaemia on ecg
Promotes cell membrane depolarisation and tachyarrhythmias
Low voltage p waves and qrs complexes, prominent u waves peaked t waves
Effects of hypermagnesaemia on ecg
Delayed av conduction, prolonged pr and wide qrs and t wave elevation
Effects of hyponatraemia on ecg
Low voltage ecg complexes
How will acidosis and alkalosis effect ecg
Produce same ecg changes as hyperkalaemia and hypokalaemia respectively.
How does systemic vascular resistance compare to pulmonary vascular resistance?
Roughly 5-7 times greater
Where does blood return to right atria from
Ivc svc and cardiac circulation
When does coronary perfusion of the lv/rv occur
Lv mainly during diastole
Rv during both systole and diastole
Phases of systole
Isovolumetric ventricular contraction
Ventricular ejection
Opening pressure of aortic valve
Max pressure in lv usually
80mmHg
120mmHg
Why does the pressure gradient reverse between the LV and aorta
LV pressure falls, aortic pressure maintained by momentum of last bit of ejected blood
What is the dicrotic notch on an arterial trace?
What about the following dicrotic wave
Closure of aortic valve and isovolumetric relaxation of lv
The wave is caused by elastic recoil of artery against closed aortic valve
What is typical end systolic lv volume
40-50ml
Usual max rv pressure
20-24mmHg
Significance of a low dicrotic notch on art trace
Suggests vasodilation as pressure gradient to close aortic valve occurring later in the cardiac cycle.
Stages of diastole
Isovolumetric relaxation
Opening of mitral valve
Rapid ventricular filling
Passive ventricular filling (diastasis)
Atrial contraction
What is the relative contributions of rapid+passive ventricular filling and atrial contraction to left ventricular end diastolic volume
75 and 25% respectively
Typical End diastolic lv volume
120ml
What is the usual gradient between lv and aortic pressures during ejection phase of systole?
1-2mmHg
When is the RA filled during the cardiac cycle
Continuous
What are LA and RA pressures caused by passive filling?
How do they change in diastole
Left 2-5mmHg
Right 0-2 mmHg
Mimic ventricular pressure in diastole as valve open
What are the atrial pressure waves?
When do they occur?
A - atrial contraction, immediately prior to systole
C - av valve bulging back into atria on contraction of ventricle
V - slow filling of atria against closed av valve causing back pressure to build
Why is myocardial relaxation considered an active process
What is the term for this phase? What influences it?
Active reuptake of calcium into SR
Lusitrophy
Influenced by increased catecholamine levels allowing heart to relax more quickly
What is the effect of incomplete reuptake of calcium into the sarcoplasmic reticulum
Diastolic dysfunction.
As heart rate increases what part of the cardiac cycle shortens first
Diastasis
What occurs to ventricular filling when hr reaches 140
Impacts on rapid filling phase compromising filling and thus stroke volume
What would cause the atrial phase of filing to be of greater importance
Myocardial ischaemia
Ventricular hypertrophy
What are the functions of chordae tendonae and papillary muscles
To prevent excessive bulging of AV valves during systole and pull base of heart towards apex
Normal aortic valve area
Mitral
2.6 to 3.5cm2
4-6cm2
Which valves have higher blood velocity and why
Semilunar valves - smaller area
What is the effect of severe aortic (70% reduction to 0.8cm2) stenosis on pressure gradient across valve
Increases markedly to >50mmHg
What contracts first, RA or LA
RV or LV
RA
LV
Which ventricle starts ejecting blood first
Rv - despite later start much lower pressure to overcome
What causes the heart sounds
Closure of valves causing vibration in ventricular walls and valve leaflets + turbulence in interrupted blood flow
Valves causing S1 heart sound
AV closure
Why would S1 heart sound be split
Mitral closes 10-30ms before tricuspid
What corresponds to s2 heart sound
Closure of SL valves
Which SL valve closes first
Aortic during inspiration due to increased venous return delaying RV ejection
Simultaneous during expiration
Cause of third heart sound
When is it heard
Heart failure due to rapid filling of dilated non compliant ventricle
Mid diastole (between s2 and s1
Cause of fourth heart sound
When heard
Conditions that cause stronger atrial contraction to assist filling ventricles
Immediately before S1
Why do you get heart murmurs
.
Blood flow usually laminar up to critical velocity
When valve narrowed velocity increases and exceeds critical velocity so turbulent flow and
murmur. When valve incompetent blood leaks backward in turbulent regurgitation
Cause of cannon a wave
Atrial contraction against closed av valve
Eg in heart block
What are the x and y descents on a cvp waveform
X - fall in rv pressure when pulmonary valve opens (ventricle moves down decreasing pressure on RA
Y - drop in atrial pressure when av valve opens
Factors that would increase cvp
Cardiac failure
Volume overload
Pericardial tamponade
Factors that would reduce cvp
Low inter vascular volume
Effect of bradycardia on cvp waveform
More distinct waves
Effect of tachycardia on cvp waveform
Fusion of c and a waves
Differentiate av junctional rhythm and complete heart block by appearance of jvp waveform
Av junctional gives regular cannon a waves
Chb gives irregular cannon a waves
Effect of tricuspid regurgitation on jvp waveform
Loss of c wave and x decent - becomes massive cv wave
Prominent v waves
What is represented by the area within the loop of a lv volume vs pressure graph
Stroke work
How would an end diastolic pressure volume relationship vary between a compliant heart and a heart with diastolic dysfunction
Compliant heart roughly linear relationship (as volume increases pressure increases gradually and linearly
In diastolic dysfunction the gradient is steeper (same change in volume is a greater change in pressure) and sudden increase in pressure with little volume change past a certain point.
What effects the gradient of an end systolic pressure volume relationship
Contractility - steeper in more contractile heart, less steep in lower contractile heart
What are the axis of a frank curve,
What does it address?
X - initial length
Y - tension
The tension of an individual muscle fibre based on initial length
Tension increases with length, initially linearly, then less effect, before shifting to decreasing tension past a certain point.
How can a frank curve be applied to cardiac muscle as a whole
(Starling curve)
The principle can be applied to the entire wall, with tension related to end diastolic volume (representing stretch or length) - increased end diastolic volume causes increased stroke volume until a point then reduces
What is the frank starling curve
Relationship between stroke volume and ventricular end diastolic volume
What causes a raised frank starling curve (higher SV for given ventricular end diastolic volume? Lower
Higher - increased contractility - positive inotropy eg adrenaline
Lower - decreased contractility - negative inotropy eg acidosis, beta blockers, hypoxia
Would a normal ventricle ever enter the decending limb of the frank starling curve
Wh?
No
Decreased compliance with increased stretch limiting max length even at very high pressures.
Define stroke volume
Volume of blood ejected from ventricle in single contraction
EDV - ESV
What is stroke index?
Normal value?
Stroke volume / body surface area
In a 70kg person 30-65ml/beat/m^2
What is ejection fraction
Stroke volume as percentage of EDV
ie ((EDV-ESV)/EDV) * 100
Gold standard methods for measuring stroke volume
Ventriculography
Cardiac Ct
mri
Radionuculotide scans
Practical methods of estimating stroke volume
Echocardiography (TOE much more accurate)
Thoracic impedance
How does thoracic impedance measure stroke volume
Measure changes in electrical impedance around neck and lower thorax
Very inconsistent and innacurate
What is cardiac index
Cardiac output divided by Body surface area
Average cardiac output and cardiac index for 70kg person
5-6 litres/min
3-3.5 litres/min/m^2
Methods of clincially measuring cardiac output
Pulmonary artery catheter (swan ganz)
LiDCO
PiCCO
Pulse contour CO vigileo
Oesophageal doppler
How does a pulmonary artery catheter measure cardiac output?
Thermodilution
Cold saline into RA and change in blood temp measured in pulmonary artery
Using a pulmonary artery catheter and thermodilution how is cardiac output calculated
Stewart Hamilton equation
Inverse proportionality to area under temperature time curve
What is the Steward Hamilton equation
Means of calculating cardiac output by thermodilution
CO = vol of injectable (initial blood temp - injectate temp) x constants. / integral of blood temp change
Advantages of co monitoring by swan ganz catheter
Can keep running pressure measurements
Can measure PA pressures and PACWP too.
Can by used with intraaortic balloon pump
Little systemic heat dissipation
“Gold standard”
Disadvantages of swan ganz catheter for CO measurements
Invasive
Risk of heart and vessel injury
Catheter can migrate
No obvious outcome benefit
Not continuous
Effects on accuracy of pulmonary artery catheter thermodilution CO measurements
Shunts
Tricuspid regurgitation
Positive pressure ventilation
How does LiDCO work to measure CO
Lithium chloride bolus into CVP and then sample arterial blood
Once calibrated with above can use arterial waveform to continuously give CO
Advantages of LiDCO in CO monitoring
No heat dissipation errors
Can be done with routine central and arterial lines
Continuously monitors
Disadvantages of LiDCO in CO monitoring
Needs 24hrly calibration
No PA pressures
Can’t be used if IABP in situ
Can’t be used in patients on lithium Tx
How does PiCCO work to measure CO
Cold saline into CVP line
Thermistor detects in a femoral a line
Once calibrated continuous art line analysis for CO
Advantages of PiCCO for CO monitoring
Continuous
Can use art line for blood sampling as well
Disadvantages of PiCCO for CO monitoring
Errors due to heat dissipation
Arterial line has to be femoral
How does pulse contour CO vigileo work to measure CO
Analysis of waveform on art line and use of demographic data to estimate
What are the advantages of pulse contour CO vigileo
Uses standard art line
No calibration needed
What are disadvantages of pulse contour CO vigileo
Uses extrapolation from patient demographic data
Depends on a line trace quality
No use if IABP in situ
How does Doppler measure CO
Oesophageal or sternal notch probe
Uses Doppler signal of blood flow in aorta and patient demographics to calculate Co
Advantages of Doppler to calculate CO
Does not require vascular access
Does not require calibration
Disadvantages of Doppler in Co monitoring
Consistency depends on trace
Cannot be used with IABP
What is Ficks principle? How can it be applied to cardiac output monitoring?
Issues
The amount of substance taken up by an organ (or body) per time is equal to arterial concentration minus the venous concentration multiplied by the blood flow.
By applying Ficks principle to oxygen concentration at a steady state cardiac output can be derived by VO2/(CaO2 -CvO2)
Oxygen uptake in the lungs over 1 min / (arterial oxygen content - venous oxygen content)
Issues are with accurate monitoring and maintaining steady state.
How does a Doppler measure cardiac output
Measures velocity of blood flow through aorta, heart rate, cross sectional area, velocity-time integral and a constant to calculate output
Main factors that determine stroke volume?
Preload
After load
Contractility
What is the definition of preload?
How can it be practically conceptualised and measured?
Presystolic length of cardiac muscle fibres
Practically considered the filling pressures of the ventricles and end diastolic volume
Practically approximated with CVP or PCWP
What factors effect preload?
Blood volume
Body position
Intrathrocaic and intrapericardial pressures
Venous tone and compliance
Pumping action of skeletal muscle
Ventricular compliance
Synchronous atrial contribution to ventricular filling
How is the conceptual preload measured practically
Can’t measure EDV so measure end diastolic pressure - this has a linear relationship to volume at normal pressures in a normal heart (edpvr) but increases as filling pressures increase or compliance fails.
Right EDP is measured with right atrial pressure or CVP
Left EDP is measured with PCWP or pulmonary starts diastolic pressure
What are the limitations of using CVP / PCWP to approximate end diastolic volume to approximate preload?!?
Ventricular compliance may not be normal (e.g. low compliance needs higher pressure for same volume)
Av valve may be abnormal (e.g. MS needing higher pressure for same volume)
Positive interthoracic pressure can transmit through to pulmonary artery catheter increasing mean PCWP (e.g. interference from PEEP)
Placement of pulmonary artery catheter in dependant part of lung could add hydrostatic pressure to PCWP signal
High pulmonary vascular resistance can lead to higher pulmonary artery diastolic pressures (e.g. pulmonary hypertension)
Definition of afterload
Practical concept, practical measure
Ventricular wall stress developed during systole
Practically considered as interventricular pressure developed during systole using SVR/PVR and MAP/MPAP as practical measures
Factors affecting afterload
Systemic/pulmonary vascular resistance
Factors stimulating or depressing cardiac contraction
Intrathoracic pressure or intrapericardial pressure
Preload
Ventricular wall thickness
Which law links ventricular wall thinkness to afterload
What is it
Laplaces law
Pressure = (2 x wall thickness x tension) / radius
How does a normal ventricle respond to afterload?
What occurs in case of a sudden increase - what is the effect termed?
Increases its performance to maintain stroke volume
Sudden afterload increase would cause fall in stroke volume with subsequent increased EDV which causes increased stroke volume - the Anrep effect
What measures can be used to determine afterload
Arterial pressure - used as a proxy for ventricular pressure
SVR / PVR
Systemic vascular impedance
Limitation of using arterial pressure to infer ventricular pressure
Inaccurate if significant gradient across av
How is SVR calculated
MAP-CVP/CO * 80 dynes.sec.cm-5
Normal range for SVR
Normal range for PVR
900-1400 dynes.sec.cm-5
90-150 dynes.sec.cm-5
Why is SVR a poor indicator of afterload
Only one component of it.
If the ventricle is contracting poorly afterload will be low no matter how high SVR
Formula for pulmonary vascular resistance
MPAP-PCWP/CO * 80 dyne.sec.cm-5
Components of systemic vascular impedance
SVR
Reactive component - compliance/elasticity of the wall - high elasticity gives higher afterload
Which wall would have a higher afterload - a thin or thick walled ventricle
Thin - higher stress for given systolic pressure
Definition of contractility
Practical concept
Systolic myocardial work done for given preload / afterload
Ejection fraction for given cvp/map
Factors effecting contractility
Increased with
Calcium levels
Sympathetic stimulation
Parasympathetic inhibition
Inotropy and digoxin
Decreased with
Opposite of above
Hypoxia and acidosis
Myocardial ischaemia and infarction.
Formulae for stroke work of the ventricle
How can it be normalised for body size
SW = stroke volume x (MAP - filling pressure)
Convert to stroke volume work index (calculated for BSA)
What is the intrinsic rate of a denervated heart
Why different to physiological resting heart rate
110
Dominant parasympathetic tone
What is the sympathetic stimulation that influences heart rate
Circulating catacholaminies
Cardiovascular reflexes via cardio accelerator nerves (T1-5)
Where are the centres responsible for cardiovascular rate control
Sympathetic and parasympathetic nuclei of the medulla
What is the parasympathetic supply to the heart, where does it originate and insert?
Dorsal motor nucleus of the vagus and nucleus ambiguus in medulla
Right and left vagus nerve
Right vagus to SA node, left to AV node
Physiological effect of vagal stimulation to the heart
Decreased slope of phase 4 and increased hyperpolarisation slowing heart rate
Sympathetic stimulation to the heart
Origin and insertion
T1-5 sympathetic chain
Stellate ganglion to all parts of heart (esp ventricular muscle)
Right side covers SA node and left AV node
Physiological effect of sympathetic stimulation to the heart
Increase slope of phase 4 increasing heart rate
Other than direct stimulation of the heart how else do the sympathetic and parasympathetic nerves influence heart rate
Inhibit one and other through direct interconnections
What cardiovascular reflexes influence heart rate?
Lung volume stretch - increase in lung volume increases heart rate
Chemoreceptor reflex - vagal stimulation slowing heart rate, offset by stimulation of resp centres
Bambridge reflex - stretch of atrial stretch receptors causes increased heart rate
Baroreceptor reflex - stretch of baroreceptors causes decreased heart rate
What is the effect of heart rate on cardiac output
Increases up to 140bpm
After 140-150bpm significant reduction in filing time overall reduces output
What occurs to contractility with increasing heart rate
Effect name
Why
Increases
Bowditch effect
Less diastolic time for reuptake of calcium so more available for contration
At what decreasing heart rate will cardiac output begin to be effected (ie. When stroke volume increases can’t overcompensate for rate)
40
