The Heart and Circulation ( 25% ) Flashcards
The most rapid conduction of electrical impulses occur in
- Atrial pathway
- AV node
- Bundle of His
- Purkinje system
- Ventricular muscle
- Atrial pathway - 1m/s
- AV node - 0.05m/s
- Bundle of His - 1m/s
- Purkinje system - 4 m/s
- Ventricular muscle - 0.3m/s
With regard to cardiac action potentials
- Cholinergic stimulation increases the slope of the pre-potential.
- The resting membrane potential is increased by X (vagal) stimulation.
- Phase O and phase I are the steepest in the AV node.
- The T wave is the surface ECG manifestation of phase I.
- The action potential in the AV node is largely due to calcium fluxes
The action potential in the AV node is largely due to calcium fluxes
- Cholinergic stimulation decreases the slope of the pre-potential.
- The resting membrane potential is decreased (hyperpolarised) by X stimulation.
- Phase O and phase I are flattest in the AV node (compared to other tissues in the heart), which is the cause of the slow conduction speeds
- The T wave is the surface ECG manifestation of repolarisation (phase 3)
The cardiac action potential is divided into 5 phases, which of the following statements are true
- Depolarization phase (0) rapid exit of Na out of cells.
- Early rapid repolarisation phase (1) drop in membrane potential to -90mV.
- Plateau phase (2) slow exit of Ca out of cell
- Terminal phase of rapid repolarisation (3) membrane potential returns to 0mV.
- Period between action potentials (4) activation of Na/K pump
- Depolarization phase (0) rapid exit of Na Into cells
- Early rapid repolarisation phase (1) drop in membrane potential to 0mV
- Plateau phase (2) slow influx of Ca Into the cell (and K+ out)
- Terminal phase of rapid repolarisation (3) membrane potential returns to -90mV
- Period between action potentials (4) activation of Na/K pump
Which of the following is false regarding the structures of the cardiac conduction system
- The SA node is located at the junction of the SVC and the R atrium
- The AV node is located in the R posterior portion of the interatrial septum
- The internodal pathways containing 3 bundles of atrial fibres that contain Purkinje type fibres
- The Purkinje type fibres are normally the only conducting pathways between the atria and the ventricles
- The bundle of His divides in a left and right bundle branch.
- The SA node is located at the junction of the SVC and the R atrium
- The AV node is located in the R posterior portion of the interatrial septum
- The internodal pathways containing 3 bundles of atrial fibres that contain Purkinje type fibres
-
The Purkinje type fibres are normally the only conducting pathways between the atria and the ventricles
- AV node is the only conducting pathway - does not have Purkinje fibres as these are for fast conduction (though these lead to and from it)
- The bundle of His divides in a left and right bundle branch (The left bundle then subdivides into anterior and posterior fascicles)
which of the following normally has the steepest prepotential
- SA node.
- AV node
- Bundle of His
- Terminals of the Purkinje fibres
- Ventricular muscle mass
SA node.
If the others had a steeper prepotential, they would spontaneously discharge faster than the SAN and would become the heart’s pacemaker
which of the following is false regarding the pacemaker function of the cardiac conducting system
- in the normal human heart each beat originates in the SA node
- the heart rate in AV nodal block is approximately 45/min
- the heart rate in infranodal block is approximately between 15-35/min
- the atrial rate in AF is higher than the ventricular rate
- the HR is independent of the respiratory cycle
- in the normal human heart each beat originates in the SA node
- the heart rate in AV nodal block is approximately 45/min
- the heart rate in infranodal block is approximately between 15-35/min
- the atrial rate in AF is higher than the ventricular rate
-
the HR is independent of the respiratory cycle
- Sinus arrhythmia - HR increases with inspiration slightly due to variation in vagal activity with respiration
Which is false
- Rhythmicity in the SA node is primarily due to increased permeability to K
- The AV node delays passage of the impulse from the atria to the ventricles by approximately 0.13s
- The velocity of electrical impulse conduction through the atria is approximately equal to that through the ventricular muscle fibres
- The transmission time from endocardial to epicardial surface is approximately equal to that of the entire Purkinje system
- Action potentials can travel both ways through all tissues of the heart except the AV node
Rhythmicity in the SA node is primarily due to increased permeability to Na and K (funny channels)
Vagal stimulation of the SA node
- Leads to increased conductance of Ca ions into the cell.
- Leads to increased conductance of K ion into the cell.
- Leads to increased intracellular cAMP.
- Decreases the slope of the prepotential (phase 4 of the cardiac action potential)
- Inhibits the β1 receptors directly.
- Slows the opening of calcium channels
- Leads to increased conductance of K ion out of the cell (efflux -> hyperpolarisation)
- Leads to decreased intracellular cAMP (opposite of NA action of beta 1 receptors)
- Decreases the slope of the prepotential (phase 4 of the cardiac action potential)
- Inhibits the β1 receptors indirectly by inhibiting pre-synaptic release of NA
Which is true
- The resting membrane potential of ventricular muscle fibres is greater than that of the SA node
- The resting membrane potential of ventricular muscle fibres is greater than that of average resting peripheral nerve fibres
- The resting membrane potential of Purkinje fibres is less than that of the AV node
- The resting membrane potential of the SA node is equal to the AV node
- The resting membrane potential of average resting peripheral nerves is less than that of the SA node
Nick says D, seem E might be right, not in Ganongs
- The resting membrane potential of ventricular muscle fibres is greater than that of the SA node
- vent - -90mV, SA -55mV
- The resting membrane potential of ventricular muscle fibres is greater than that of average resting peripheral nerve fibres
- -90mV vs -70mV
- The resting membrane potential of Purkinje fibres is less than that of the AV node
-
The resting membrane potential of the SA node is equal to the AV node
- -55mV
- Have read SA = -50-60 and AV = -60-70
- The resting membrane potential of average resting peripheral nerves is less than that of the SA node
- -70mV vs -55mV
- ?this is right
Which is correct
- ACh increases cardiac conducting system fibres’ permeability to K which increases the slope of phase 4 and so increases the heart rate
- Noradrenaline increases Na and Ca permeability therefore increases HR by decreasing the negativity of the resting membrane potential and by increasing the slope of phase 4 (prepotential)
- The AV node and the Purkinje fibres do not function as the cardiac pacemakers because background X stimulation reduces their rate of firing to below the rate of the SA node.
- Nicotinic receptors in the SA node are responsible for increasing the resting HR in smokers.
- None of the above
- ACh increases cardiac conducting system fibres’ permeability to K (true) which decreases the slope of phase 4 and so decreases the heart rate
- Noradrenaline increases Na and Ca permeability therefore increases HR by decreasing the negativity of the resting membrane potential and by increasing the slope of phase 4 (prepotential)
- The AV node and the Purkinje fibres do not function as the cardiac pacemakers because Overdrive suppression means they fire at a fast rate than their innate rate - ie they are excited externally before they have a chance to reach their internal depol threshold
- Nicotinic receptors in the SA node are responsible for increasing the resting HR in smokers - wrong
- Nicotinic receptors (being parasympathetic) would cause bradycardia
Carotid sinus massage sometimes stops SVT because
- It decreases sympathetic discharge to the SA node
- It increases X discharge to the SA node
- It increases X discharge to the conducting tissue between the atria and the ventricles
- It decreases sympathetic discharge to the conducting tissue between the atria and the ventricles
- It increases the refractory period of the ventricular myocardium
It increases X discharge to the conducting tissue between the atria and the ventricles (aka the AVN)
- Carotid sinus afferent is IX -> NTS -> vagal afferents.*
- Vagal afferents act on the SAN (right vagus) and AVN (left vagus) to reduce HR and slow AVN conduction*
- Note aortic arch afferents are vagal*.
In this situation, slowing the SAN would not help, need to block the AVN to stop the arrhythmia.
In the cardiac action potential
- Initial rapid depolarization is due to opening of voltage gated K channels.
- Phase 2 is due to opening of Na channels.
- Phase 3 is due to the opening of K channels
- Extracellular potassium concentration is not important
- The magnitude is affected by external sodium concentration
The magnitude is affected by external sodium concentration
- Initial rapid depolarization is due to opening of voltage gated Na channels
- Phase 2 is due to opening of Ca channels
- Phase 3 is due to the opening of K channels
- Extracellular potassium concentration is not important
cardiac muscle contraction
- is in its absolute refractory period in the latter half of phase 3 and phase 4
- shows decrease in the number of cross bridges between actin and myosin (during descending limb of Starling’s curve)
- shows greater inotropism when catecholamines act on β1 adrenergic receptors
- shows increased contraction when digoxin stimulates Na/K ATPase.
- in Duchenne’s muscular dystrophy, shows hypertrophy but does not lead to cardiac failure
- is in its relative refractory period in the latter half of phase 3 and phase 4
- ARR is phase 0-> part way through 3
- shows increase in the number of cross bridges between actin and myosin (during descending limb of Starling’s curve)
-
shows greater inotropism when catecholamines act on β1 adrenergic receptors
- ie sympathetic B1 stimulation -> increased inotropy (duh)
- shows increased contraction when digoxin inhibits Na/K ATPase.
- Less Na efflux -> less Na/Ca cotransport -> maintain higher intracellular Ca concentrations
- in Duchenne’s muscular dystrophy, shows hypertrophy but does not lead to cardiac failure??
regarding conduction in the heart
- stimulation of right X inhibits the AV node.
- the rate of discharge of the SA node is independent of temperature.
- depolarization of ventricular muscle starts on the right.
- the speed of conduction is fastest in ventricular muscle.
- the SA node and the AV node exhibit the same speed of conduction
- stimulation of right X inhibits the SA node. (right = SA, left = AV)
- the rate of discharge of the SA node is dependent on temperature.
- hypothermia->bradycardia
- depolarization of ventricular muscle starts on the left
- the speed of conduction is fastest in Purkinje fibres
- the SA node and the AV node exhibit the same speed of conduction
In the cardiac action potential
- The resting membrane potential is -70mV.
- The initial depolarization is due to Ca influx.
- The plateau is due to the IKI current.
- The initial rapid repolarisation is due to the closure of Na channels
- cAMP decreases the active transport of Ca to the sarcoplasmic reticulum thus accelerating relaxation and shortening of the cycle
- The resting membrane potential is -90mV
- The initial depolarization is due to Na influx.
- The plateau is due to the Calcium influx (ICa) current.
-
The initial rapid repolarisation is due to the closure of Na channels
- Partly, also the opening of K+ channels
- cAMP decreases the active transport of Ca to the sarcoplasmic reticulum thus accelerating relaxation and shortening of the cycle
- ???increases number of fast Ca channels available -> faster influx of Ca
With respect to cardiac muscle action potential
- As HR increase the QRS duration decreases
- The absolute refractory period last from phase 0 to half way through phase 4.
- Relative refractory period begins halfway through phase 3
- Phase 1 is due to opening of voltage gated Na channels.
- Voltage gated Ca channels are activated at -50mV.
- As HR increase the QRS duration decreases - wrong
- The absolute refractory period last from phase 0 to half way through phase 3
- Relative refractory period begins halfway through phase 3
- Phase 1 is due to closure of voltage gated Na channels.
- Phase 0 is opening of voltage gated Na channels
- Voltage gated Ca channels are activated at 0-20mV
With respect to depolarization of the heart
- Atrial depolarization is complete in 100 ms
- AV nodal delay is 10 ms.
- AV nodal delay is lengthened by increasing sympathetic stimulation.
- Ventricular muscle depolarizes from the right
- The last area to be depolarized is the posterobasal portions of the RV
- Atrial depolarization is complete in 100 ms
- AV nodal delay is 160ms
- AV nodal delay is lengthened by increasing parasympathetic stimulation.
- Ventricular muscle depolarizes from the left
- The last area to be depolarized are the posterobasal portions of the left ventricle, the pulmonary conus, and the uppermost portion of the septum
The rate of the pacemaker cells in the heart can be slowed by all of the following except
- More negative diastolic potential
- Reduction of the slope of diastolic depolarization
- More positive threshold potential
- Prolongation of the action potential
- Increased phase 4 depolarisation slope
Increased phase 4 depolarisation slope
Lower slope = longer time to depol
action potential initiation in the SA and AV nodes results from
- Na influx
- K influx
- Ca influx
- Na and Ca influx
- Increased K conductance
Calcium influx
Only in the SA and AV nodes
All other muscle is Na
with respect to the cardiac action potential
- the plateau of repolarisation phase may be up to 200 times longer than the depolarization phase
- unlike the nerve action potential, there is no overshoot
the plateau of repolarisation phase may be up to 200 times longer than the depolarization phase
the slowest conducting type of cardiac tissue is
- bundle of His
- ventricular muscle
- Purkinje system
- Atrial pathway
- AV node
AV node
The action potential of cardiac pacemaker cells
- Is not affected by calcium current
- Is mainly due to sodium influx
- Shows decreased prepotential slope with sympathetic stimulation
- Exhibits a prepotential initially caused by decreased K efflux
- Show no spontaneous rhythmicity
- Is not affected by calcium current
- T channels open and allow Ca influx to finish the prepotential, then L channels open and produce the AP
- Is mainly due to calcium influx
- Shows increased prepotential slope with sympathetic stimulation
- Exhibits a prepotential initially caused by decreased K efflux
- Show no spontaneous rhythmicity
- All cardiac cells have spontaneous rhythmicity, at different rates
With regard to the 12 lead ECG
- Lead II is at 90 degrees for vector analysis.
- 130 degrees is still a normal cardiac axis.
- the standard limb leads record the potential difference between 2 limbs
- V2 is placed in the 3rd interspace.
- Septal Q waves are predictable in V2.
- Lead II is at 120 degrees for vector analysis.
- 130 degrees is Right axis
- Normal is -30 - +110
- 130 degrees is Right axis
- the standard limb leads record the potential difference between 2 limbs
- V2 is placed in the 4th interspace (same for V1-3), 5th for V4
- Septal Q waves are not predictable in V2.
- No Q-wave in V1-2 (ie QRS is initially an upward deflection as septum depolarises from left to right and therefore towards V1 and 2)
- Q-wave represents septal depolarisation, and V1+2 look at the septum directly, so do not record a voltage change
Which of the following is false regarding the waves of the ECG
- The P wave is produced by atrial depolarization
- The Q wave is produced by atrial repolarisation
- The QRS complex is produced by ventricular depolarization
- The T wave is produced by ventricular repolarisation
- The U wave is probably produced by slow repolarisation of the papillary muscle
The Q wave is produced by septal depolarisaiton (hence is not seen in the septal leads V1+2)
Which of the following is false regarding physiological ECG intervals
- The duration of the P wave is normally < 0.1s
- The duration of the QRS complex is normally < 0.1s
- The duration of the PQ interval ranges between 0.12-0.2 s and is dependent on the frequency
- The QT interval starts with the end of the Q and ends with the beginning of the T wave and has an average duration of 0.4s
- The average duration of the ST interval is 0.32s
The QT interval starts with the end of the Q and ends with the beginning of the T wave and has an average duration of 0.4
QT is start of the Q to end of the T, average duration 0.4, up to 0.43
Which of the following regarding the cardiac vector is false?
- The normal direction of the mean QRS vector is normally between -30 and +110
- The mean QRS vector is indicating the electrical axis of the heart
- The QRS vector can be calculated from any 2 standard limb leads
- In LBBB the mean QRS vector is > +110.
- The mean electrical axis is dependent on respiration and on the position of the body
In LBBB the mean QRS vector is > +110.
LBBB causes LAD, so vector is <-30
Which of the following is true regarding the electrical axis of the heart
- LAD, highest QRS lead I, negative QRS lead II
- LAD, highest QRS lead I, positive QRS lead II
- RAD, highest QRS lead III, negative QRS aVR
- RAD, negative QRS lead III, negative QRS aVR
- The electrical axis of the heart can be calculated from any unipolar chest lead
LAD, highest QRS lead I, negative QRS lead II
- LAD - +ve I, -ve II, III
- Any negative II = LAD
- RAD - +ve III, aVF, -ve I, +/- II
- Positive aVF, negative I
Which ECG leads reflect the anterior surface of the heart
- I, aVL, V5-6
- II, III, aVF
- V1-4
- V1-2
- I, II, aVR
V1-2
as per Nick
But V1-4 seem to be known as the anteroseptal leads
Regarding the ECG
- The U wave is believed to be due to papillary muscle repolarisation
- The PR interval is the time taken for atrial repolarisation
- Lead III is the vector between the right arm and left leg
- LBBB is defined by cardiac axis > 30 degrees
- Lead V5 is placed in the 4th ICS MCL
- The U wave is believed to be due to papillary muscle repolarisation
- The PR interval is the time taken for atrioventricular conduction
- Lead II is the vector between the right arm and left leg
- III is left arm to left leg
- LBBB is defined by cardiac axis < -30 degrees
- Lead V5 is placed in the 5th ICS
- V1-3 4th ICS, 4-6 5th ICS
The normal ECG
- The average QT is 450ms
- There is no Q wave in V1
- The normal axis is between -10 and 110 degrees
- T wave coincides with the diastolic blood pressure
- P wave coincides with the venous a wave
There is no Q wave in V1
- The average QT is 400ms (up to 430ms)
- The normal axis is between -30 and 110 degrees
- T wave coincides with late systole - contraction lasts longer than the AP
- P wave immediately precedes the venous a wave (which correspons to the atrial systole) - electrical activity slightly precedes the corresponding mechanical activity
During the ST segment of the ECG, there is
- No current flow, all myocardial membranes positive outside, negative inside
- Normal current flow of repolarisation
- Inability of damaged myocardium to depolarize if ST segments are elevated
- Current flow if other than on zero potential line
- If elevated, current flow during diastole
Inability of damaged myocardium to depolarize if ST segments are elevated
- Delayed depolarisation can cause ST elevation (systolic current of injury), as this causes a moment of the exterior of infarcted cells to be relatively more positive than healthy cells (but depends on their classification of ‘inability’ vs ‘delayed’. An inability to polarise can also cause TQ depression, which manifests as an ST elevation on ECG.*
- Thus, STE can be due to delayed depolarisation, or an inability to polarise (ie RMP close to 0). They cannot get stuck in a polarised state.*
or
Current flow if other than on zero potential line
This is a basic tenet of ECGs I’m fairly sure.
- No current flow, all myocardial membranes positive outside, negative inside
- ST represents the plateau phase of the AP - maintained by Ca2+ influx to balance the K+ efflux which is aiming to repolarise the cell, so there is current flow, it is just balanced.
- Normal current flow of repolarisation
- See above - ST is plateau phase, T-wave represents current flow of depolarisation
- If elevated, current flow during diastole
- ST segment occurs during systole (diastole is the T-P segment), so it has nothing to do with diastolic current flow
The R wave of the ECG is due to
- Ca influx
- Cl influx
- Na influx
- K efflux
- Cl efflux
Na influx
QRS = ventricular depol = Na influx
T-wave = ventricular repol = K+ efflux
atrial flutter is characterized by
- an atrial rate slower than the ventricular rate.
- flutter waves with a saw tooth appearance
- an atrial rate between 160-240 bpm.
- doesn’t occur with an AV block.
- carotid sinus massage can’t convert atrial flutter into the normal SR.
- an atrial rate much faster than the ventricular rate (2:1 or 3:1)
- flutter waves with a saw tooth appearance
- an atrial rate between 200 to 350 (usually 300)
- Almost always occurs with AV block
- carotid sinus massage can sometimes convert atrial flutter into the normal SR.
- ACh release at vagal nerve endings depresses conduction of atrial myocytes
Which is false regarding AF
- Can be cardioverted by electrocardioversion
- Can cause acute heart failure
- Causes reduction in CO due to loss of the atrial kick
- Can be caused by hypothyroidism
- The ventricular rate can be lowered by digitalis die to its depression on AV conduction
Can by caused by _Hyper_thyroidism
The absence of conduction of electrical impulses through the AV node, bundle of His or bundle branches, characterized by independent beating of the atria and ventricles is called
- SSS
- 2nd degree, type I block
- 3rd degree block
- 1st degree block
- 2nd degree, type II block
3rd degree block
Which is false regarding AV block
- 1st degree block is characterized by abnormally long PR intervals >0.2s and constant
- 2nd degree, type I (Wenckebachs) is characterized by progressive lengthening of the PR interval until a QRS complex fails to appear after a P wave
- 2nd degree, type II block is characterized by regularly or irregularly absent QRS complexes
- 3rd degree block is caused by a complete block of electrical impulses in one bundle branch and an intermittent block in the other bundle branch
- 3rd degree block can cause Adams Stokes syndrome due to intermittent ventricular asystole
3rd degree block is caused by a complete block of electrical impulses in one bundle branch and an intermittent block in the other bundle branch
Is a constant complete block of all bundles
In 2nd degree heart block
- The ventricular rate is lower than the atrial rate
- The ventricular ECG complexes are distorted
- There is a high incidence of VT
- Stroke volume is decreased
- CO is increased
The ventricular rate is lower than the atrial rate
What is false regarding the effect of K on the ECG
- ST segment depression is a sign of low K
- QT interval is prolonged in low K > 2.5
- Tall peaked T waves in high K are a sign of altered repolarisation
- In low K < 3.5 mmol/L a prominent U wave can be found
- In sever high K > 8.5 the P wave disappears
QT interval is prolonged in low K > 2.5
Which is false regarding the ECG changes in MI
- ST elevation of >1mm in limb leads is considered significant for MI
- ST depression of >1mm below baseline is considered a sign for severe myocardial ischaemia
- ST elevation of >0.5mm in chest leads is considered significant for MI
- An abnormal Q wave (>0.04 s wide, depth > ¼ height of succeeding R) is considered a sign of irreversible myocardial necrosis
- Acute LBBB is frequently caused by an anteroseptal MI
ST elevation of >0.5mm in chest leads is considered significant for MI
Criteria varies but usually about 2-3mm in V2-3 depending on age and gender
What is false regarding the effects of electrolytes on the heart
- Low Ca causes prolonged ST segment and the QT interval
- High K is more rapidly fatal than low K
- Mg counteracts digitalis toxicity
- High K enhances digitalis toxicity
- Changes in Na concentration has no significant effect on the heart
Low K enhances digitalis toxicity
Digoxin binds to the extracellular K+ site of Na-K-ATPase, so hypokalaemia reduces potassiums antagonistic effects on digoxin. Likewise hyperkalaemia can reduce the risk of toxicosis.
Note digoxin toxictiy can cause hyperkalaemia (due to reduced intake into cells due to Na-K-ATPase inhibition).
Magnesium suppresses digoxin-induced ventricular arrhythmias
With regard to the cardiac cycle
- Phase I represents atrial systole
- The aortic valve opens at the beginning of phase II
- The T waves of the ECG occur during phase IV
- The 2nd heart sound is due to mitral closure
- The C wave is due to tricuspid opening.
- Phase I represents atrial systole
- The aortic valve opens at the end of phase II.
- Phase 2 = isovolumetric ventricular contraction
- The T waves of the ECG occur during phase III (ejection)
- The 2nd heart sound is due to Aortic valve closure
- The C wave is due to Tricuspid bulging into the RA during isovolumetric contraction
The c wave in the JVP is due to
- The rise in atrial pressure before the tricuspid valve opens in diastole
- Transmitted pressure due to tricuspid bulging in isovolumetric contraction
- Atrial systole
- Atrial contraction against a closed tricuspid valve in complete heart block
- The increase in intrathoracic pressure during expiration
Transmitted pressure due to tricuspid bulging in isovolumetric contraction
a = atrial sysole
V = rise in atrial pressure before triscupid opens in diastole
During the valsalva manoeuvre bradycardia occurs
- At the onset of straining
- As the intrathoracic pressure reaches a maximum
- As a result of an initial increase in CO
- When the glottis is opened and intrathoracic pressure returns to normal
- If the patient has autonomic insufficiency
When the glottis is opened and intrathoracic pressure returns to normal
Initial rise in BP due to brief increase in venous return, but then raised intrathoracic pressure causes the venous return to fall -> reduced BP -> tachycardia + baroreceptor mediated vasocontriction.
Once glottis is opened, the venous return and CO return to normal, but the vasoconstriction is still in place -> hypertension. This is sensed by baroreceptors -> bradycardia.
Which is false regarding the cardiac cycle
- During late diastole, the tricuspid and mitral valves are open
- About 70% of the ventricular filling occurs passively during diastole
- Isovolumetric contraction starts with the opening of the aortic and pulmonary valves
- Isovolumetric relaxation ends when the ventricular pressure falls below the atrial pressure and the tricuspid and mitral valves open
- When the HR is increased the duration of diastole is shortened
Isovolumetric contraction starts with the opening of the aortic and pulmonary valves
starts with closing of mitral and tricuspid valves
Which of the following is false regarding the cardiac cycle
- The atrial systole starts after the P wave of the ECG
- The ventricular systole starts near the end of the R wave of the ECG
- The ventricular systole end just after the T wave of the ECG
- The systolic pressure in the vascular system refers to the peak pressure reached during systole
- The diastolic pressure in the vascular system refers to the peak pressure reached during diastole
The diastolic pressure in the vascular system refers to the peak pressure reached during diastole
Refers to low point (or maybe stable pressure)
Which is false
- The dicrotic notch in the aortic pressure curve is caused by the closure of the aortic valve
- Venous pressure is lower during inspiration than during expiration
- The a wave in the JVP is due to atrial systole
- The c wave in the JCP is produced by the bulging of the tricuspid valve into the atria
- The v wave is caused by the rise in atrial pressure due to the closing of the tricuspid valve
The v wave is caused by the rise in atrial pressure due to the closing of the tricuspid valve
V wave = release of the slow rise in atrial pressure during diastole due to opening of the triscuspid valve
The fourth heart sound is caused by
- Closure of the aortic and pulmonary valves
- Vibrations in the ventricular wall during systole
- Ventricular filling
- Closure of the mitral and tricuspid valves
- Regurgitant flow in the vena cava
Ventricular filling
1st = closure of AV valves
2nd = closure of aortic/pulmonary valves
3rd = rapid ventricular filling causing vibrations
4th = ventricular filling when atrial pressure is high or ventricle is stiff (not usually normal)
During the cardiac cycle
- Systole is the period of ventricular contraction (ie between the 1st and 2nd heart sounds).
- The SV is increased by increasing the EDV, not the EF
- Ventricular contraction commences at the R wave and is not completed until the end of the T wave
- Diastole is the period between opening and closure of the AV valves
- JVP waves occur at – a atrial systole, c ventricular systole, v just prior to opening the AV valves.
- Systole is the period of ventricular contraction (ie between the 1st and 2nd heart sounds).
- 2nd heart sound is just after the beginning of diastole, as momentum keeps blood flowing for a split second after contraction finishes so the valve is still open.
- The SV is increased by increasing the EDV, not the EF
- can be increased by either (increased inotropy -> increased contraction -> increased EF)
- Ventricular contraction commences at the R wave and is not completed until the end of the T wave
- Diastole is the period between opening and closure of the AV valves
- Systole begins a fraction before closure of the AV valces
- JVP waves occur at – a atrial systole, c ventricular systole, v just prior to opening the AV valves.
- Notes that v ‘mirrors the rise in atrial pressure just before the tricuspid valve opens during diastole’
- Incorrect part could also be they want c to be isovolumetric contraction of ventricles, rather than systole in general
In the cardiac cycle
- Right ventricular contraction occurs before the left
- Phase II commences with the opening of the AV valves
- Phase IV is isovolumetric relaxation
- During inspiration the pulmonary valves close before the aortic
- The duration of systole is more variable than diastole
- Right ventricular contraction occurs after the left
- Phase II commences with the closing of the AV valves
- II = isovolumetric contraction
- Phase IV is isovolumetric relaxation
- During inspiration the pulmonary valves close after the aortic
- increased pulmonary resistance in inspiration causes a slight delay in pulmonary valve closure, the same reason splitting can occur in PE
- The duration of systole is more consistent than diastole
Regarding the heart sounds
- The 3rd heart sound is heard 1/3 way through diastole in many normal young individuals
- A 4th heart sound can be heard in some individuals with low atrial pressure
- The 1st heart sound is loud when the heart rate is slow
- The interval between the aortic and pulmonary valves is decreased during inspiration
- The 2nd heart sound is normally lower pitched and longer than the first
- The 3rd heart sound is heard 1/3 way through diastole in many normal young individuals
- A 4th heart sound can be heard in some individuals with high atrial pressure, or stiff ventricles (eg LVH)
- The 1st heart sound is soft when the heart rate is slow
- Because ventricles are well-filled and the AV valve leaflets float together before systole
- The interval between the aortic and pulmonary valves is increased during inspiration
- Because of increased resistance in pulmonary circuit (same as PE)
- The 2nd heart sound is normally higher pitched and shorter than the first
with respect to the cardiac cycle and the ECG
- the start of systole is marked by the P wave
- the PR interval represents atrial relaxation
- the ST segment represents absolute refractory period of the ventricles.
- the T wave is synchronous with the third heart sound
- none of the above
None of the above
- the start of systole is just after the P wave
- the PR interval represents atrial contraction
- Atrial repolarisation (ie the atrial t-wave) is buried in QRS complex
- the ST segment represents absolute refractory period of the ventricles. ARP is from the start of the QRS to the apex of the T-wave
- the T wave is well before the third heart sound
- T-wave is just before diastole begins, third heart sound is 1/3rd through diastole
- T-wave ends just before 2nd heart sound
CO is decreased by
- Sleep.
- Eating.
- Pregnancy in the 1st trimester.
- Sitting from a lying position.
- All of the above
- Sleep - No change
- Eating - Increases
- Pregnancy in the 1st trimester - Increases
- Sitting from a lying position - Due to reduced venous return
myocardial contractility is decreased by all except
- acidosis
- barbiturates
- hypercarbia
- bradycardia.
- glucagon
glucagon.
Activates adenylyl cyclase -> increased cAMP -> therefore increases magnitude of calcium release
Tachycardia increases inotropy due to reduced diastolic time creating less time to remove calcium from cytoplasm -> higher cytosolic calcium -> increased inotropy (Force-Frequency Relationship)
Bradycardia would have the opposite effect of above
Though CO could remain similar if EDV was raised through increased diastolic time
CO is increased by
- Sleep
- Moderate change in environmental temperature
- Eating
- Rapid arrhythmia
- Sitting or standing from lying position
Eating
Myocardial contractility is decreased by
- Acidosis
- Quinidine.
- Hypoxia
- Hypercapnia
- All of the above
All of the above
Acidosis, hypercapnia, hypoxia through reduced ATP -> impaired SR Ca release + downregular of beta receptors
Quinidine is a Class Ia anti-arrhythmic -> blocks voltage-gated calcium channels (like verapamil)
Which of the following regarding volumes of the cardiac cycle is false
- EDV is ~ 130mL
- ESV is ~ 20mL.
- SV is ~ 70-90mL in a resting man of average size in the supine position
- EF is the % of the ventricular volume ejected with each stroke
- SV in AF can be reduced up to 20%.
ESV is ~ 70mL
SV in AF can be reduced up to 20% - Atrial contraction contributes up to 30% of ventricular filling, and this may be partially lost in AF
Which of the following regarding pressures is false
- RAP is ~ 10-15mmHg.
- Peak LVP is about ~120mmHg
- Peak RVP is about 25mmHg
- CVP is about 0-8mmHg
- Pulmonary arterial pressure is about 5-25mmHg
RAP is ~ 5mmHg.
Same as CVP (approx. 5mmHg)
Which is false
- RAP resembles CVP
- The wedge pressure resemble LAP
- RAP resembles RVEDP
- SV = CO/HR
- Diastolic pressure in the left ventricle is about 40-80mmHg.
Diastolic pressure in the left ventricle is < 10mmHg
Regarding CO, which is false
- In a resting, supine man ~ 5.0L/min
- Can be measured with the direct Fick method
- Is dependent on preload, contractility, afterload and HR
- Can be calculated CO = VO2/CaO2-CvO2
- Pregnancy decreases CO.
Pregnancy increases CO.
During exercise a man consumes 1.8 L of oxygen per minute. His arterial oxygen content is 190mL/L and the oxygen content of his mixed venous blood is 134mL/L. His CO is approximately
- 3.2L/min
- 16L/min
- 32L/min
- 54L/min
- 160mL/min
32L/min
LV output
= O2 consumption (ml/min) / [AO2] - [VO2]
=1800mL/min / 56ml/L
= 32L/min
Starling’s law of the heart
- Does not operate in the failing heart
- Does not operate during exercise
- Explains the increase in the HR produced by exercise
- Explains the increase in the CO that occurs when venous return is increased
- Explains the decrease in the EDV when venous return is increased
Explains the increase in the CO that occurs when venous return is increased
‘states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant’
or
‘the heart will pump all blood returned to it’
Starling’s law describes the relationship of
- HR/SV
- HR/EDV
- Afterload/EDV
- SV/EDV
- Preload/SV
SV/EDV
The Frank Starling curve, which is false:
- Describes the myocardial contractility
- Is shifted upwards and to the left during increased preload
- Is shifted upwards and to the left during increased afterload.
- Is shifted downwards and to the right in cardiac insufficiency
- Is shifted upwards and to the left during noradrenaline administration
Is shifted upwards and to the left during increased afterload.
This is false, the rest are true
The EDV
- Is increased by increased total blood volume
- Is decreased by AF.
- Is decreased by an increased CVP.
- Is decreased in cardiogenic shock.
- Is decreased when standing
Is decreased when standing
As per Nick
However AF will reduce ventricular filling by the atria and hence EDV
EDV only reduces upon standing from sitting/lying, not if you are already standing.
Is decreased in septic or hypovolaemic shock.
Is increased by an increased CVP or total blood volume
The work performed by the left ventricle is substantially greater than that performed by the right ventricle, because in the left ventricle
- Contraction is slower
- The wall is thicker
- The SV is greater
- The preload is greater
- The afterload is greater
The afterload is greater
RAP
- May fall to as little as -10mmHg at rest, but rarely more
- May be 6cm of blood normally
- Will tend to fall with venoconstriction.
- Increases with exercise
- Increases with inspiration
- May fall to as little as -10mmHg at rest, but rarely more
- May be 6mmHg of blood normally
- Will tend to rise with venoconstriction.
- Increases with exercise
- Cannot find anything on RAP in exercise - LAP will initially rise before falling to normal or subnormal values
- Decreases with inspiration (as increased intrathoraic pressure reduces venous return)
Which is true
- Starlings law of the heart explains homometric regulation of CO
- Compliance is reduced by scarring resulting in reduced heterometric response to preload
- Afterload promotes sarcomeres shortening while preload opposes it
- β1 receptor stimulation results in further sarcomeres shortening and ultimately to increased CO
- increased venous tone decreases the myocardial sarcomeres length
Compliance is reduced by scarring resulting in reduced heterometric response to preload
Heterometric = changes in CO regulated by changes in cardiac muscle fibre length
Homometric = changes in CO due to increased contractility independent of length
- Starlings law of the heart explains heterometric regulation of CO
- Afterload promotes sarcomeres shortening while preload opposes it
- ??
- β1 receptor stimulation results in further sarcomeres shortening and ultimately to increased CO
- ??
- increased venous tone increases the myocardial sarcomeres length
- Due to increased venous return
The EF represents
- The % blood remaining in the ventricle following systole
- The % of atrial volume ejected into the ventricles with atrial systole
- Aortic blood flow
- The % of ventricular volume ejected with each stroke
- LVP
The % of ventricular volume ejected with each stroke
Regarding the CO, which is false
- Resting CO correlates with the body surface area
- CO is not affected by moderate changes in environmental temperature
- Heterometric regulation is changing contractility of the heart muscle fibres independent of length.
- The output per square metre of body surface is the cardiac index
- CO is not affected by sleep
Homometric regulation is changing contractility of the heart muscle fibres independent of length.
Heterometic = changing length, ie Frank-Starling law
decrease in the length of ventricular cardiac muscle fibres can be brought about by
- Stronger atrial contraction
- Increase in total blood volume
- Increase in venous tone
- Standing
- Increase in negative intrathoracic pressure
Standing
Reduced length of cardiac fibres seems to be another way of saying reduced EDV / preload
Regarding the cardiac cycle
- SV is normally 50mL
- Contraction of the left atrium precedes the right atrium
- The c wave of the JVP corresponds to movement of the closed tricuspid valve
- LVP immediately falls after opening of the aortic valve
- At rapid heart rates, systole shortens more than diastole
- SV is normally 70ml
- Contraction of the left atrium follows the right atrium
- The c wave of the JVP corresponds to movement of the closed tricuspid valve
- LVP immediately falls after opening of the aortic valve
- Wrong, increases slightly then falls a bit, but only really falls once the aortic valve closes (needs to be at least 80mmHg to keep it open)
- At rapid heart rates, systole shortens much less than diastole
Isovolumetric ventricular contraction
- Is responsible for the venous v wave
- Causes rapid rise in intraventricular pressure
- Lasts half a second
- Causes the opening of the AV valves
- Decreases the atrial pressure
- Is responsible for the venous C wave
- Causes rapid rise in intraventricular pressure
- Lasts about 0.05sec
- Causes the closing of the AV valves
- Slightly increases the atrial pressure by causing a bulging of the valves into them
the CO
- is correlated with body surface area
- is a product of the HR and EDV
- can be calculated by using p-aminohippuric acid
- is decreased during sleep
- is decreased during eating
is correlated with body surface area
About 3.2L / min / m2 BSA
- is a product of the HR and SV
- can be calculated by using radioactive isotopes or themodilution
- is unchanged during sleep
- is increased during eating
All of the following factors may increase EDV except
- Maximal inspiration
- Hypervolaemia
- Exercise
- Standing up
- Adrenaline
Standing up
Blood pools in legs and reduces venous return -> reduced EDV
which of the following is true concerning the heart
- increased volume of work is the product of heart rate and stroke volume
- cardiac work is the product of HR and SV
- the heart in its resting state gains 60% of its caloric requirements from FFAs
- the work of the left ventricle is twice that of the right due to higher pressures in the systemic circulation
- increased preload has a greater effect on O2 consumption of the heart than increased afterload
- increased volume of work is the product of MAP and stroke volume
- cardiac work is the product of MAP and SV
- the heart in its resting state gains 60% of its caloric requirements from FFAs
- the work of the left ventricle is 6-7x that of the right due to higher pressures in the systemic circulation
- increased afterload has a greater effect on O2 consumption of the heart than increased preload
- For unclear reasons, pressure-work produces a greater increase in O2 consumption than volume-work
Which of the following does not cause an increase in CO
- Eating
- Moderate increase in environmental temperature
- Pregnancy
- Exercise
- Anxiety
Moderate increase in environmental temperature
concerning venous pressure, which is false
- because sagittal sinus veins have rigid walls and cannot collapse, the pressure in the upright position is sub-atmospheric
- the CVP is normally 4-6mmHg, but varies with respiration
- CVP rises during negative pressure breathing
- Elevated CVP occurs with expanded blood volume
- Peripheral venous pressure rises with increasing distance from the heart
CVP falls during negative pressure breathing
NPB seems to be akin to an iron lung - ie negative extrathoraic pressure. This would presumably cause dilation of the IVC etc and reduce CVP.
PEEP -> increase in CVP