Cardiovascular Physiology Flashcards
What is a cardiac cycle?
The time for one systole and one diastole. If the HR was 80bpm then a cardiac cycle would last 0.75s
How much time is diastole and systole? How does this alter in faster HRs?
1/3 systolic 2/3 diastolic It becomes 50:50 at faster HRs to allow max time for stroke volume ejection but compromises time for diastolic filling and coronary perfusion
How does the resistance against which the left side of the heart has to eject compare to the right?
The SVR is 5 times higher than the pulmonary vascular resistance (PVR).
How does the normal peak left ventricle pressure compare to the right?
LV is 120mmHg and right is 25mmHg
What are the sequence of events following diastole?
- Isovolumetric relaxation
- Ventricular filling (Rapid -> slow (diastasis)
- Atrial systole
- Systole
- Isovolumetric contraction
- Ventricular systole
What are on the x and y axes of the pressure-time curve when describing the left ventricle pressure changes during the cardiac cycle?
X-axis = time (seconds)
Y-axis = pressure (mmHg)
What does the pressure time curve look like for the left ventricle?
What does the pressure-time curve look like for the aorta/left atrium and ECG?
Describe the events during cardiac systole and how they relate to the pressure-time changes on the graph
- atrial systole
- reflected pressure from atrial ejection into the ventricles
- MV closes
- atrial systole completes ventricular filling
- pressure in LV > LA so MV closes
- isovolumetric contraction
- both MV + AV closed, 1st stage of systole
- represents pressure generation which stops when LV pressure > aortic pressure and AV opens, sharp upstroke in pressure
- AV opens
- at 80 mmHg
- Ejection
- ventricular ejection into aorta
- AV closes
- as ejection continues, pressure falls in LV
- isovolumetric relaxation
- both MV + AV closed
- first stage of diastole
- relaxation is metabolically active
- MV opens
- MV opens as LV pressure falls below LA, passive ventricular filling commences
Describe the pressure-time changes in the aorta
- AV opens
- when pressure in LV exceeds that of aorta (80mmHg)
- Ejection
- initially rapid then slows
- AV closes
- when the LV pressure is < aortic pressure the AV closes
- pressure then falls in aorta due to diastole due to run off into vascular tree
- elastic recoil of aortic walls creates a dichrotic notch on the aortic pressure trace
Describe the pressure-time changes in the left atrium
- a wave
- atrial contraction delivering 30% of volume to LV
- c wave
- isovolumetric contraction, bulging back of MV into LA so small increase in pressure
- x descent
- as the ventricle contracts this pulls the fibrous atrio-ventricular rings towards the heart apex
- this comparitively lengthens the atria and causes pressure to fall
- v wave
- LA pressure rises due to venous return accumulating the atria throughout systole whilst the MV is closed
- y descent
- MV opens, blood flows into ventricle
- pressure in LA falls
What does AF cause on the pressure-time changes of the left atrium?
No a waves
What does tricuspid regurg look like on the pressure-time change curve of the left atrium?
- prominent v
- loss of c wave
- loss of x descent
What causes a regular cannon “a” on the pressure time curve of the left atrium?
AV junction block
What causes an irregular cannon “a” on the pressure time curve of the left atrium?
Complete heart block
What does the pressure-volume loop for the left ventricle look like?
- shows the volume of blood “moved” by the pump and how much pressure is generated to achieve this
- this represents one cardiac cycle
- volume (mls) on the x axis
- pressure (mmHg) on the y axis
- A = MV opens
- B = MV closes
- C = AV opens
- D = AV closes
- B - C = isovolumetric contraction
- D - A = isovolumetric relaxation
- stroke volume = LVEDV - LVESV
- work done = pressure x volume (area inside of loop)
What is pre-load and how does it affect the pressure volume loop of the heart?
- preload is the end diastolic stretch or tension of the ventricular wall
- signified by the left ventricular end diastolic volume on the x-axis
- at increased LV volumes the shape of the LV filling curve changes from linear to a gradually increasing gradient
- increasing preload increases SV until overdistension occurs (frank-starling relationship)
What is elastance?
The slope of the pressure volume loop curve = the change in pressure/change in volume
This is elastance (reciprocal of compliance)
What is contractility in the heart?
The intrinsic ability of the heart to do mechanical work for a given pre- and afterload.
It’s shown by the slope of the end-systolic pressure line.
This contractility line is known as Ees.
If contractility increases then Ees has an increased slope and is therefore rotated up and to the left eg; if catecholamines administered.
What is afterload? How does this affect the pressure-volume loop?
Afterload is the ventricular wall tension required to eject the stroke volume. It is indicated by slope of straight line joining LVEDV from x-axis to the end systolic point of the loop (Ea).
If afterload increases in isolation then the gradient of line moves up and to the right.
What is normal coronary blood flow?
200-250 ml/min (adult) or 5% of cardiac output
What is the O2 extraction of the heart?
High (55-60%) compared to the rest of the body as a whole (25%)
What is coronary perfusion pressure?
The driving pressure for the coronary circulation generated by the difference between aortic pressure and intracardiac pressures.
During diastole = aortic diastolic pressure - LV end diastolic pressure
Why does left coronary blood flow cease during systole?
Left coronaries are exposed to considerable pressure from LV during systole. This compresses them to stop flow.
Flow in the coronaries to the right ventricle and atria will still occur as intra-cavity transmitted pressures are lower.
What part of the ECG corresponds with the first heart sound?
The P wave occurs before the 1st heart sound - this signifies atrial depolarisation which triggers atrial systole
What part of the cardiac cycle does the R wave on an ECG coincide with?
The ventricular isovolumetric contraction - this occurs when the mitral and aortic valves are closed
The pressure generating phase occurs with ventricular contraction coupled with excitation contraction coupling
Where are diastolic pressures higher - the pulmonary artery or the right ventricle?
The pulmonary artery.
Pressures are typically 25/15 mmHg in the pulmonary artery vs 25/8 mmHg in the right ventricle.
When does isovolumetric relaxation end?
When the atrial pressure exceeds the ventricular pressure
Isovolumetric means both the inflow and outflow valves for that chamber are closed, hence the volume cannot change. When the pressure in the ventricle falls below that of the atria then the mitral valve will open and blood will flow down its pressure gradient to commence ventricular filling.
What pressure does the left atrium typically reach at the onset of atrial systole?
10mmHg
What wave is atrial contraction associated with?
A wave
What % of ventricular filling is atrial systole responsible for?
30% (lost in AF)
What waves are associated with heart block?
Cannon waves
There is dissociation between atrial and ventricular contraction and the atria contract against a closed tricuspid/mitral valve
What causes exaggerated v waves?
Tricuspid regurgitation.
The ‘v’ wave is formed by passive filling of the atria. Regurgitant blood flowing back into the atria across the tricuspid valve increases the volume in the atria and exaggerates the ‘v’ wave.
When does the x wave occur?
The ‘x’ is a descent which corresponds to (falling pressure within the atria during) atrial relaxation. This occurs during ventricular systole where ventricular muscle contraction pulls the atrio-ventricular rings towards the apex of the heart, this “lengthens” the atria and causes pressure to fall within the atria.
How does the immediate endocardial layer obtain O2?
From diffusion from blood within the cavity ie not reliant on coronary perfusion
What is the most significant determinant of coronary blood flow to the left ventricle?
Coronary blood flow to the LV occurs predominantly in diastole, therefore:
Aortic DIASTOLIC pressure - intracardiac pressure (LVEDP)
How is stroke volume calculated?
LV end diastolic volume - LV end systolic volume = mls ejected from the ventricle
What does the area inside the pressure-volume loop for the left ventricle represent?
The work done by the ventricle
What does increasing preload do to the pressure-volume loop?
Moves it up and to the right because it increases the volume in the LV.
What line can be drawn on the pressure-volume loop of the heart to indicate afterload?
Slope of a line made by joining the left ventricular end diastolic volume with the end-systolic point on a pressure-volume loop.
What does administration of catecholamines do to the Ees contractility line?
It increases the gradient of the line, so it rotates upwards towards the y-axis
What is an action potential?
It describes the sequential changes in membrane potential which result in propagation of an electrical impulse. These changes occur due to alterations in membrane permeability and movement of ions through channels.
What is the resting membrane potential?
RMP is the transmembrane voltage that exists when an excitable cell is quiescent (not producing an AP) and is negative inside with respect to the outside the cell.
What factors contribute to the RMP?
- Na/K ATPase - 3Na+ are pumped out, 2K+ in (net loss of 1 negative charge per pump cycle)
- the membrane is 100x more permable to K+ than Na+
- there are negatively charged molecules inside the cell (proteins and phosphate) - Donnan effect
What is automaticity?
It’s a property of the cardiac pacemaker cells which means it lacks a stable RMP and spontaneously decays towards threshold.
At threshold an all or nothing depolarisation is initiated.
What are the rates of spontaneous discharge at the SA, AV nodes and of ventricular cells?
SA node - 70-80/min
AV node - 60/min
Ventricular cell - 40/min
What is the maximum negative potential of cardiac pacemaker cells?
- 60 mV
What is the threshold potential of cardiac pacemaker cells?
-40 mV
What is the peak positive potential of cardiac pacemaker cells?
+20 mV
What is the duration of cardiac pacemaker cells?
150ms
What are the phases of the cardiac pacemaker cell AP?
- Phase 4 “pre-potential”
- no stable RMP
- slow decrease in membrane permeability to K+
- this moves RMP from -60 mV to -40mV (threshold)
- slope of pre-potential determines HR
- Phase 0 “depolarization”
- due to Na+ influx and a small contribution from Ca2+
- slow response from AP - less steep slope and slower rise than in Phase 0 of a ventricular muscle cell
- Phase 3 “repolarization”
- due to inactivation of slow Ca2+ channels and increased K+ outflow
How does stimulation of the sympathetic nervous system affect the cardiac pacemaker AP?
INcreases the slope of the pre-potential hence increased HR
What effect does parasympathetic stimulation have on the cardiac pacemaker AP?
Increased K+ efflux in Phase 4 - thus delaying the pre-potential reaching threshold. Therefore slope is reduced and HR slowed.
What is the maximum negative potential for a ventricular muscle cell?
- 90mV
What is the threshold for a ventricular muscle cell?
- 70 mV
What is the peak positive potential for a ventricular muscle cell?
+ 20mV
What is the duration of a ventricular muscle cell AP?
200 ms
What are the phases in a ventricular muscle cell AP?
- Phase 0 - rapid depolarization
- fast Na+ channels open at threshold -70mV and Na+ pours into cell down conc + electrical gradient
- Phase 1 - spike
- onset of depolarization due to Na+ channel closure
- Phase 2 - plateau
- small current of Ca2+ into cell through slow-L type calcium channels
- opening at -35mV
- timed inactivation
- essentially balances the efflux of K+ so potential stays positive
- this provides the absolute refractory period and prevents tetany
- Phase 3 - repolarization
- closing of calcium channels + large efflux K+
- Phase 4 - RMP
- stable diastolic potential
- maintained by differential permeability of membrane to K+ vs Na+ (100:1) and 3Na:2K ATP pump
What is excitation-contraction coupling?
The sequence of events that convert an electrical impulse (AP) to mechanical force (cardiac muscle contraction).
How does excitation contraction coupling work?
- The cardiac muscle cell membrane (sarcolemma) forms invaginations (T-tubules) which transport the AP into the cell
- Depolarization triggers opening of voltage gated L-type Calcium channels
- Calcium then stimulates ryanodine receptors on the SR surface so that calcium floods out the SR into the cell. Calcium induced calcium release (CICR).
- Calcium binds to the C-subunit of troponin (TnC).
- Tropomyosin rotates and exposes myosin binding sites on actin (Trop I is bound to actin). Actin and myosin bind (needs ATP) - sarcomere shortens - muscular contraction.
- At the end of the pleateau calcium levels fall
- reuptake into SR (ATP dependent)
- timed inactivation of L-type channels
- export of calcium out of cell by sodium-calcium exchange pump
What is a typical resting sarcomere length?
2.2 μm
What does Trop I and Trop T bind to?
Trop I binds to Actin
Trop T binds to Tropomyosin
What effect does beta adrenergic stimulation have on calcium flow through the L type channels?
It increases the calcium flow - thus generating positive inotropy
