The Heart and Circulation ( 25% ) Flashcards

1
Q

The most rapid conduction of electrical impulses occur in

  • Atrial pathway
  • AV node
  • Bundle of His
  • Purkinje system
  • Ventricular muscle
A
  • Atrial pathway - 1m/s
  • AV node - 0.05m/s
  • Bundle of His - 1m/s
  • Purkinje system - 4 m/s
  • Ventricular muscle - 0.3m/s
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2
Q

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
A

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)
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3
Q

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
A
  • 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
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4
Q

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.
A
  • 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)
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5
Q

which of the following normally has the steepest prepotential

  • SA node.
  • AV node
  • Bundle of His
  • Terminals of the Purkinje fibres
  • Ventricular muscle mass
A

SA node.

If the others had a steeper prepotential, they would spontaneously discharge faster than the SAN and would become the heart’s pacemaker

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6
Q

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
A
  • 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
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7
Q

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
A

Rhythmicity in the SA node is primarily due to increased permeability to Na and K (funny channels)

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8
Q

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.
A
  • 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
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9
Q

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
A

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
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10
Q

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
A
  • 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
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11
Q

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
A

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.

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12
Q

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
A

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
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13
Q

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
A
  • 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??
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14
Q

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
A
  • 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
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15
Q

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
A
  • 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
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16
Q

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.
A
  • 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
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17
Q

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
A
  • 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
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18
Q

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
A

Increased phase 4 depolarisation slope

Lower slope = longer time to depol

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19
Q

action potential initiation in the SA and AV nodes results from

  • Na influx
  • K influx
  • Ca influx
  • Na and Ca influx
  • Increased K conductance
A

Calcium influx

Only in the SA and AV nodes

All other muscle is Na

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20
Q

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
A

the plateau of repolarisation phase may be up to 200 times longer than the depolarization phase

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21
Q

the slowest conducting type of cardiac tissue is

  • bundle of His
  • ventricular muscle
  • Purkinje system
  • Atrial pathway
  • AV node
A

AV node

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22
Q

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
A
  • 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
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23
Q

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.
A
  • Lead II is at 120 degrees for vector analysis.
    • 130 degrees is Right axis
      • Normal is -30 - +110
  • 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
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24
Q

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
A

The Q wave is produced by septal depolarisaiton (hence is not seen in the septal leads V1+2)

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25
Q

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
A

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

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26
Q

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
A

In LBBB the mean QRS vector is > +110.

LBBB causes LAD, so vector is <-30

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27
Q

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
A

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
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28
Q

Which ECG leads reflect the anterior surface of the heart

  • I, aVL, V5-6
  • II, III, aVF
  • V1-4
  • V1-2
  • I, II, aVR
A

V1-2

as per Nick

But V1-4 seem to be known as the anteroseptal leads

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29
Q

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
A
  • 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
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30
Q

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
A

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
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31
Q

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
A

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
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32
Q

The R wave of the ECG is due to

  • Ca influx
  • Cl influx
  • Na influx
  • K efflux
  • Cl efflux
A

Na influx

QRS = ventricular depol = Na influx

T-wave = ventricular repol = K+ efflux

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33
Q

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.
A
  • 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
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34
Q

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
A

Can by caused by _Hyper_thyroidism

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35
Q

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
A

3rd degree block

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36
Q

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
A

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

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37
Q

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
A

The ventricular rate is lower than the atrial rate

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38
Q

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
A

QT interval is prolonged in low K > 2.5

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39
Q

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
A

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

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40
Q

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
A

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

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41
Q

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.
A
  • 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
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42
Q

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
A

Transmitted pressure due to tricuspid bulging in isovolumetric contraction

a = atrial sysole

V = rise in atrial pressure before triscupid opens in diastole

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43
Q

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
A

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.

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44
Q

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
A

Isovolumetric contraction starts with the opening of the aortic and pulmonary valves

starts with closing of mitral and tricuspid valves

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45
Q

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
A

The diastolic pressure in the vascular system refers to the peak pressure reached during diastole

Refers to low point (or maybe stable pressure)

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46
Q

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
A

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

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47
Q

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
A

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)

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48
Q

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.
A
  • 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
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49
Q

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
A
  • 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
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50
Q

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
A
  • 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
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51
Q

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
A

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
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52
Q

CO is decreased by

  • Sleep.
  • Eating.
  • Pregnancy in the 1st trimester.
  • Sitting from a lying position.
  • All of the above
A
  • Sleep - No change
  • Eating - Increases
  • Pregnancy in the 1st trimester - Increases
  • Sitting from a lying position - Due to reduced venous return
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53
Q

myocardial contractility is decreased by all except

  • acidosis
  • barbiturates
  • hypercarbia
  • bradycardia.
  • glucagon
A

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

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54
Q

CO is increased by

  • Sleep
  • Moderate change in environmental temperature
  • Eating
  • Rapid arrhythmia
  • Sitting or standing from lying position
A

Eating

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55
Q

Myocardial contractility is decreased by

  • Acidosis
  • Quinidine.
  • Hypoxia
  • Hypercapnia
  • All of the above
A

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)

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56
Q

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%.
A

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

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57
Q

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
A

RAP is ~ 5mmHg.

Same as CVP (approx. 5mmHg)

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58
Q

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.
A

Diastolic pressure in the left ventricle is < 10mmHg

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59
Q

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.
A

Pregnancy increases CO.

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60
Q

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
A

32L/min

LV output

= O2 consumption (ml/min) / [AO2] - [VO2]

=1800mL/min / 56ml/L

= 32L/min

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61
Q

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
A

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’

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62
Q

Starling’s law describes the relationship of

  • HR/SV
  • HR/EDV
  • Afterload/EDV
  • SV/EDV
  • Preload/SV
A

SV/EDV

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63
Q

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
A

Is shifted upwards and to the left during increased afterload.

This is false, the rest are true

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64
Q

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
A

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

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65
Q

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
A

The afterload is greater

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66
Q

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
A
  • 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)
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67
Q

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
A

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
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68
Q

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
A

The % of ventricular volume ejected with each stroke

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69
Q

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
A

Homometric regulation is changing contractility of the heart muscle fibres independent of length.

Heterometic = changing length, ie Frank-Starling law

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70
Q

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
A

Standing

Reduced length of cardiac fibres seems to be another way of saying reduced EDV / preload

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71
Q

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
A
  • 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
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72
Q

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
A
  • 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
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73
Q

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
A

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
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74
Q

All of the following factors may increase EDV except

  • Maximal inspiration
  • Hypervolaemia
  • Exercise
  • Standing up
  • Adrenaline
A

Standing up

Blood pools in legs and reduces venous return -> reduced EDV

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75
Q

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
A
  • 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
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76
Q

Which of the following does not cause an increase in CO

  • Eating
  • Moderate increase in environmental temperature
  • Pregnancy
  • Exercise
  • Anxiety
A

Moderate increase in environmental temperature

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77
Q

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
A

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

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78
Q

regarding Frank-Starling curves

  • the extent of afterload is proportionate to end diastolic volume.
  • cardiac muscle fibres are lengthened by decreased ventricular compliance
  • contractility of myocardium is increased on standing
  • sympathetic stimulation shifts the length/tension curve upward and to the right – upward and to the left
  • increased negative intrathoracic pressure increases contractility
A
  • the extent of ?stroke volume is proportionate to end diastolic volume.
  • cardiac muscle fibres are lengthened by ?increased ventricular compliance
  • contractility of myocardium is increased on standing
    • Drop in preload/EDV -> drop in BP -> decreased baroreceptor stimulation -> decreased inhibition of RVLM -> increased sympathetic response -> increased HR and contractility
  • sympathetic stimulation shifts the length/tension curve upward and to the left
  • increased negative intrathoracic pressure increases venous return to the heart/EDV/preload
    • ​This increases CO through the F-S mechanism but does not change the contractility of the myocardium per se.
79
Q

1 Regarding ECG changes, which is CORRECT?

  • a) hypernatraemia is associated with low voltage complexes
  • b) the first change in hyperkalaemia is prolongation of QRS
  • c) with hypokalaemia, the resting membrane potential decreases
  • d) in hyperkalaemia, the heart stops in systole
  • e) in hypercalcaemia, myocardial contractility is enhanced
A
  • a) hypernatraemia is associated with high voltage complexes
  • b) the first change in hyperkalaemia is peaked T-waves
  • c) with hypokalaemia, the resting membrane potential increases (hyperpolarises)
  • d) in hypercalcaemia, the heart stops in systole
    • ​due to being unable to relax (calcium rigor)
    • Hyperkalaemia causes the heart to stop in diastole as the fibres become unresponsive to excitation
  • e) in hypercalcaemia, myocardial contractility is enhanced
80
Q

2 Regarding jugular pressure waves:

  • a) the ‘v’ wave denotes the increased atrial pressure due to the bulging of the tricuspid valve during isovolumetric ventricular contraction
  • b) in tricuspid insufficiency, there is a giant ‘A’ wave with each ventricular systole
  • c) atrial premature beats produce an ‘A’ wave
  • d) the ‘v’ wave occurs during systole
  • e) a giant ‘C’ wave (‘cannon wave’) may be seen in complete heart block
A

c) atrial premature beats produce an ‘A’ wave

A = wave produced by atrial contraction (occurs in late diastole)

C = bulging of triscupid during contraction (early systole, at end of isovolumetric contraction)

V = slow rise in atrial pressure due to inflow of blood, release once AV valves open (peaks at end of isovolumetric relaxation / end of systole)

81
Q

3 What factor does not alter cardiac output?

  • a) standingup
  • b) sleeping
  • c) eating
  • d) exercising
  • e) pregnancy
A

b) sleeping

82
Q

The greatest percentage of the circulating blood volume is contained in the

  • Capillaries
  • Larger arteries
  • Venules and veins
  • Pulmonary circulation
  • The heart
A

Venules and veins = 50%

Heart chambers = 12%

Pulmonary circulation = 18%

Aorta = 2%

Arteries = 8%

Arterioles = 1%

Capillaries 5%

Following transfusion <1% is distributed into the arterial system

83
Q

The Poiuselle – Hagen formula tells us

  • Longer tubes can sustain high flow rates.
  • Flow is directly proportional to resistance.
  • Flow will be doubled by a 20% increase in vessel diameter.
  • Why the venous capacitance system is important in CO.
  • Turbulent flow is predicted in high velocity vessels.
A

Poiselle-Hagen formula relates resistence to viscosity and tube diameter.

The main point to take away is that small changes in vessel diameter have large effects on resistence/flow as it is inversely proportional to the radius^4

  • Longer tubes cannot sustain high flow rates - More resistance so more energy losses
  • Flow is inversely proportional to resistance
  • Flow will be doubled by a 20% increase in vessel diameter
  • Turbulent flow is predicted in high velocity vessels -> this is Reynolds formula
84
Q

All of the following explain venous blood flow except

  • Intrathoracic pressure variations
  • The pumping action of the heart
  • Skeletal muscle contraction
  • Oncotic pressure gradient
  • Smooth muscle contraction
A

Oncotic pressure gradient

This only explains interstitial fluid movements/gradients

85
Q

The flow in a blood vessel is

  • Inversely proportional to the radius.
  • Inversely proportional to the pressure difference between the arterial and venous end.
  • Inversely proportional to the length.
  • Proportional to the diameter.
  • Proportional to the viscosity
A
  • Proportional to the radius (r^4).
  • Directly proportional to the pressure difference between the arterial and venous end.
  • Inversely proportional to the length.
  • Proportional to the radius^4
  • Inversely proportional to the viscosity.
86
Q

With respect to arterial pressure

  • Pulse pressure is the difference between arterial and venous pressure.
  • In the lying position the arterial pressure in the foot is higher than the arterial pressure in the head.
  • Dicrotic notch is causes by the closure of the AV valves.
  • Dicrotic notch is not present in the pulmonary circulation.
  • Pulmonary arterial pressure is approximately 25/10 mmHg
A
  • Pulse pressure is the difference between Systolic and diastolic BP
  • In the lying position the arterial pressure in the foot is lower than the arterial pressure in the head.
    • Will be lower as further from heart and no effect of gravity
  • Dicrotic notch is causes by the closure of the aortic valve
    • Low-point in BP curve between systole and the elastic effects of the aorta
  • Dicrotic notch is not present in the pulmonary circulation.
  • Pulmonary arterial pressure is approximately 25/10 mmHg
87
Q

The lumen diameter of vessels, heart chambers and alveoli is important because

  • Resistance is inversely proportional to the square of the radius.
  • The wall tension necessary to balance transmural pressure is inversely proportional to the radius.
  • Velocity is equal to flow for any given diameter.
  • Flow and resistance are both related reciprocally to the radius to the power of 4.
  • Alveoli collapse in the absence of surfactant because their diameter decreases in expiration and the wall tension increases.
A

Alveoli collapse in the absence of surfactant because their diameter decreases in expiration and the wall tension increases.

  • P=T/r, or T=P x r*
  • Where T tends to be constant, so if r decreases, you will need more pressure to balance the tension to prevent collapse (and that doesnt happen - the smaller alveoli tend to collapse into the larger ones once the tension overcomes whatever pressure is inside them, as pressure and tension should be roughly equal for all alveoli)*
  • Resistance is inversely proportional to Radius4
  • The wall tension necessary to balance transmural pressure is directly proportional to the radius (P = T/r)
  • Velocity is equal to flow for any given diameter.
    • Velocity is speed (distance/time), flow = volume/time
  • Flow is related directly to the radius to the power of 4; resistence reciprocally.
88
Q

Regarding blood flow

  • In the blood vessels is normally turbulent
  • Turbulent flow is silent.
  • The small arteries and arterioles are referred to as the capacitance vessels.
  • The average velocity of blood is highest in the capillaries.
  • Blood flow and resistance in vivo are markedly affected by small changes in the caliber of vessels
A

Blood flow and resistance in vivo are markedly affected by small changes in the caliber of vessels

  • In the blood vessels is normally Laminar
  • Turbulent flow is Loud
  • The small arteries and arterioles are referred to as Resistance vessels
    • ​Venous system is known as capacitance vessels
  • The average velocity of blood is highest in the Aorta
    • ​Flow is greatest in the capillaries
89
Q

The law of La Place predicts the following except

  • Increased myocardial work in dilated cardiomyopathy
  • The protection of capillaries against rupture
  • The relationship between transmural tension and wall tension
  • The pattern of intravesical pressure/volume curve
  • The failure of alveoli to collapse in expiration.
A

The failure of alveoli to collapse in expiration.

  • In a sphere, P = 2T/r (where P = distending (intraluminal pressure) and T = tension)*
  • If T does not reduce when r reduces, tension overcomes the distending pressure causing collapse.*
  • The only reason they do not is alveolar surfacant.*
  • The equation is viewed from a differing point with regards to capillary rupture - T = Pr, so for a smaller radius, there is less tension in the walls for a given pressure, reducing risk of rupture*
  • Increased myocardial work in dilated cardiomyopathy
    • as increased wall tension is needed to generate a given pressure if the radius is increase
  • The protection of capillaries against rupture
    • smaller radius means less wall tension is needed
  • The relationship between transmural tension and wall tension
    • I guess this is the general point of the law
  • The pattern of intravesical pressure/volume curve
90
Q

all of the following are true for venule walls except

  • are slightly thinner than capillaries
  • are thin and easily distended
  • contain relatively little smooth muscle
  • venoconstriction is caused by noradrenergic nerves and NA
  • all are correct
A

are only slightly thicker than capillaries

They are thin and easily distended, with relatively little smooth muscle

Considerable venoconstriction is caused by the activity in the NA nerves to the veins and by circulating endothelins.

91
Q

Which is incorrect regarding the biophysical characteristics of blood flow

  • It can be easily measured using Poiseulle-Hagen formula, even though blood is not a perfect fluid
  • Viscosity is a function of the haematocrit
  • Blood flow is normally laminar
  • Velocity is proportion to flow divided by the area
  • Critical closing pressure occurs when capillary pressure exceeds tissue pressure
A

Critical closing pressure occurs when capillary pressure falls below tissue pressure

92
Q

Which is incorrect

  • The law of LaPlace explains the difference between intraluminal and transmural pressure
  • The smaller the radius of a blood vessel the lower the wall tension to balance distention pressure
  • Veins are referred to as capacitance vessels and arterioles as resistance vessels
  • The recoil effect in blood vessels is known as Windkessel effect
  • The mean pressure is the average pressure in the cardiac cycle and is calculated as diastolic pressure plus 1/3 pulse pressure
A

The law of LaPlace explains the relationship between tension in the wall of a cylinder, the transmural pressure, and the radius of the cylinder/sphere

P=T/r

93
Q

concerning the capillaries, which is false

  • 5% circulating blood is in the capillaries at any one time
  • transport of substances from the capillaries into the tissues occurs via fenestrations, vesicular transport and cytoplasmic transport
  • the rate of transport along a capillary depends on Starling forces
  • oncotic and filtration pressure gradients are the same for all capillaries
  • transit time from arteriolar end to venular end averages 1-2 s
A

oncotic and filtration pressure gradients are the same for all capillaries

Varies tissue to tissue

94
Q

All the following regarding lymphatics are true except

  • The normal lymph flow is 2-4L/d
  • The 2 types of lymph vessels are interstitial and collecting.
  • Collecting lymphatics have valves and smooth muscles in their walls
  • Flow in the collecting lymphatics is aided by skeletal muscle movements
  • Functions of the lymphatics are recycling of protein and transport of long chain FFA
A

The 2 types of lymph vessels are initial and collecting.

95
Q

The volume of fluid in interstitial space is dependent on all of the following except

  • Capillary pressure
  • Capillary filtration coefficient
  • The cross sectional area of the capillary bed
  • The ratio of pre-capillary to post capillary venular resistance
  • The oncotic pressure
A

The cross sectional area of the capillary bed

(though note that Ganongs mentions ‘number of active capillaries’ as an important factor)

All other factors listed are directly quoted from Ganongs

96
Q

causes of increased interstitial fluid volume and oedema include all except

  • arteriolar constriction and venular dilation.
  • increased venous pressure
  • decreased plasma protein level
  • venous obstruction
  • substance P
A

arteriolar constriction and venular dilation.

This would reduce the hydrostatic pressure in the capillary lumen

97
Q

factors increasing blood flow through the venous system includes which

  • fluctuations in negative pressure during expiration.
  • intra-abdominal pressure rises during expiration due to abdominal muscle contraction.
  • the absence of valves in the system.
  • contractions of skeletal muscle
  • the high cross-sectional area of the great veins
A

contractions of skeletal muscle

  • fluctuations in negative pressure during Inspiration
  • Intra-abdominal pressure rises in inspiration as the diaphragm flattens. This promotes venous return to the heart as the valves in the leg veins prevent retrograde flow
  • the absence of valves in the system - Do not increase blood flow, just prevent retrograde flow
  • the high cross-sectional area of the great veins - relatively low compared to total CSA of the capillaries and venules etc
98
Q

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
A

CVP falls during negative pressure breathing (inspiration)

Negative intrathoracic pressure allows the IVC to open a bit (less interstitial pressure) so the pressure inside falls.

99
Q

lymph flow

  • on average 500mL/h into the circulation.
  • proportional to interstitial fluid pressure
  • increased with decreased interstitial fluid protein.
  • decreased with contraction of muscles.
  • decreased with raised capillary pressure.
A

proportional to interstitial fluid pressure

True if they are talking about flow in lymphatic vessels, rather than flow of fluid from blood vessels -> lymph

  • on average 124mL/h into the circulation.
    • 3L per 24 hrs = 125mL/hr
  • decreased with decreased interstitial fluid protein
    • Will reduce flow into interstium
  • increased with contraction of muscles.
    • Same as veins (muscle pump)
  • increased with raised capillary pressure.
    • Will promote increased diffusion from capillary -> interstitium
100
Q

regarding Starling forces operating in the capillaries

  • there is a net outward force of about 0.3mmHg.
  • the filtration co-efficient describes the rate of plasma proteins being filtered from the microcirculation.
  • rate of filtration is roughly equal in the different tissues of the body.
  • mean capillary pressure is normally greater than plasma colloid osmotic pressure
  • lymphatics play no role in maintaining equilibrium of the forces.
A

mean capillary pressure is normally greater than plasma colloid osmotic pressure

  • Net outward force changes between capillaries
    • Typical net filtration pressure might be 11mmHg out at the arterial end and 9mmHg inward at the venous end
  • the filtration co-efficient describes the rate of plasma proteins being filtered from the microcirculation.
    • Is something to do with the way the capillary wall acts as a filter
  • rate of filtration varies wildly in the different tissues of the body
  • lymphatics play a large role in maintaining equilibrium of the forces - increased interstitial fluid pressure leads to increased lymph flow to balance it
101
Q

Pouiselle’s equation states

  • Flow is proportional to density
  • Viscosity multiplied by flow is proportional to the pressure gradient
  • Flow is inversely proportional to the radius
  • Flow is not related to the length of the tube
  • Flow is proportional to the radius
A

Viscosity multiplied by flow is proportional to the pressure gradient

Flow is proportional to r4, and is inversely proportional to the length of the tube.

nF = (Pa - Pb) x stuff

Where n=viscosity

102
Q

regarding blood vessels

  • arterioles have a lower ratio of smooth muscle to diameter than have large arteries.
  • capillary flow is regulated by precapillary sphincters and meta-arterioles
  • capillaries have the largest cross-sectional area
  • capillaries contain 8% of the total blood volume
A

capillaries have the largest cross-sectional area

  • arterioles have a higher ratio of smooth muscle to diameter than have large arteries.
  • capillary flow is regulated by arterioles
  • capillaries contain 5% of the total blood volume
103
Q

what is common to all capillary beds?

  • All are patent
  • Are 10-20mm in diameter
  • Have a continuous basement membrane
  • Have intracellular fenestrations
A

Have a continuous basement membrane

A lot of capillary beds are collapsed at any one time in resting tissue

Are frickin small - not 10-20mm

Most have intracellular fenestrations but some (?CNS) do not, and have a tight barrier to diffusion.

104
Q

with regard to lymph

  • has no clotting factors
  • its protein content depends on the area it is from
  • is not dependent on the colloid pressure of the capillaty
A

its protein content depends on the area it is from

105
Q

flow through a narrow tube is proportional to

  • viscosity
  • length
  • average pressure in the tube
  • pressure gradient
A

pressure gradient

Inversely proportional to viscosity and length

106
Q

Oedema can be caused by

  • Raised capillary hydrostatic pressure
  • Reduced colloid osmotic pressure
  • Vitamin C deficiency
  • Elevated angiotensin II levels
  • All of the above
A

All of the above

107
Q

Air embolism

  • Cannot occur in bone
  • Affects only skeletal muscle and joints
  • Causes focal ischaemia
  • Is unlikely to occur with 10cc of air
  • Is due to dissolved oxygen in divers
A

Causes focal ischaemia

108
Q

Oedema can be caused by

  • Decreased hydrostatic pressure
  • Sodium retention
  • Hyperproteinaemia
  • Polycythaemia
  • Hypertension
A

Sodium retention

109
Q

vascular compliance

  • is equal to increase in pressure divided by increase in volume
  • is the same as vascular distensibility
  • is 24 times greater in a vein than a corresponding artery
  • is increased by sympathetic stimulation in the arterial system
  • is increased by sympathetic stimulation in the venous system
A
  • s equal to increase in pressure divided by increase in volume – C = ΔV/ΔP
  • is the same as vascular distensibility - Compliance is a measure of the tendency of a hollow organ to resist recoil toward its original dimensions upon removal of a distending or compressing force. It is the reciprocal of “elastance”. Distensibility is simply the ability to stretch and hold more volume. They are related, but not the same.
  • is 24 times greater in a vein than a corresponding artery
  • is increased by sympathetic stimulation in the arterial system - decreased
  • is increased by sympathetic stimulation in the venous system – decreased
110
Q

Regarding Starling s forces

  • Capillary pressure at the arteriole end is 15mmHg
  • Hydrostatic pressure exceeds oncotic pressure throughout the capillary
  • Capillary pressure at the venule end is 5mmHg
  • Interstitial colloid osmotic pressure is usually negligible
  • Capillary filtration coefficient decreases with capillary permeability.
A
  • Capillary pressure at the arteriole end depends but around 30mmHg
  • Hydrostatic pressure exceeds oncotic pressure at the arterial end
    • ​Example oncotic pressure is 25mmHg, hydrostatic might be 37 at arterial and 17 at venule
  • Capillary pressure at the venule end depends but around 15mmHg
  • Interstitial colloid osmotic pressure is usually negligible
  • Capillary filtration coefficient increases with capillary permeability.
111
Q

concerning capillary fluid exchange

  • venule constriction reduces filtration pressure
  • hypoproteinaemia decreases fluid shift out of capillaries
  • lymphoedema fluid has a low protein count
  • substance P increases capillary permeability
  • kinins reduce capillary permeability
A
  • venule constriction increases filtration pressure
  • hypoproteinaemia increases fluid shift out of capillaries
    • Reduced plasma oncotic pressure; hypoalbuminaemia -> oedema
  • lymphoedema fluid has a high protein count
    • caused by inadequate lymph draininage
  • substance P increases capillary permeability
    • after noxious stimuli, via the axon reflex
  • histamine and bradykinin increase capillary permeability
112
Q

with respect to baroreceptors

  • barcoreceptor stimulation causes bradycardia and a drop in BP
  • impulses generated in the baroreceptors excite the tonic discharge of vasoconstrictor nerves
  • impulses generated in baroreceptors inhibit the X innervation of the heart
  • positive pressure ventilation has no effect on Baroreceptor discharge
  • any drop in systemic arterial pressure increases the inhibitory discharge in the buffer nerves and there is a compensatory rise in BP
A

barcoreceptor stimulation causes bradycardia and a drop in BP

Afferents from the aortic arch (X) and carotid sinus (IX) terminate in the NTS -> CVLM -> RVLM (inhibited by GABA from CVLM) -> drop in BP and bradycarida

Used for short-term changse in BP (eg standing up)

113
Q

All of the following produce vasodilation except

  • Local K accumulation
  • Systemic hypoxia
  • Lactate
  • Increase CO2 tension
  • Decreased pH
A

Systemic hypoxia

Hypoxia of the RVLM will cause an increase in BP as it tries to increase blood flow to itself

Local hypoxia will cause vasodilation also

114
Q

All of the following factors will cause vasodilation in skeletal muscle except

  • Nitric oxide
  • Acidosis
  • Potassium
  • Adenosine
  • Lactate
A

Adenosine

Adrenaline causes vasocontriction most places except the hepatic, skeletal, and brain where it dilates

115
Q

Angiotensin II

  • Has less aldosterone effects as angiotensin III.
  • Increases diastolic BP
  • Penetrates the BBB
  • Has the same pressor activity of angiotensin I
  • Excess angiotensin II upregulates AT1A receptors
A

Increases diastolic BP

Increases water intake and increases retention of sodium and water -> increased plasma volume

  • Has the same aldosterone effects as angiotensin III
    • (Angiotensin III has 40% of the pressor activity of angiotensin II, but 100% of the aldosterone-producing activity)
  • Has more pressor activity than angiotensin I
    • Angiotensin I does not seem to have any biologic activity and exists soley as a precurser to Ang2
116
Q

With respect to the vasomotor centre of the brain

  • Increased Baroreceptor discharge causes increased X discharge from the vasomotor area
  • A decrease in vasomotor discharge causes an increase in systemic vascular resistance.
  • Neurons synapse with the preganglionic neurons in the lateral white columns of the spinal cord.
  • Is inhibited by input from the carotid chemoreceptor.
  • Is excited by input from the aortic baroreceptors.
A
  • Increased Baroreceptor discharge causes increased X discharge to and fromthe vasomotor area
    • X carries afferents to the vasomotor area. Increased baroreceptor discharge causes increase firing of X -> CVLM, which then releases GABA to inhibit the RVLM.
    • X carries parasympathetic efferents to the heart, which causes ACh release and via M2 (Gi linked -> reduce cAMP-> K influx -> hyperpolarisation and bradycaria)
  • A decrease in vasomotor discharge causes an decrease in systemic vascular resistance.
  • Neurons synapse with the preganglionic neurons in the Intermediolateral gray column of the spinal cord.
    • Axons of the RVLM descend in the lateral column of the spinal cord to the thoracolumbar intermediolateral gray column
  • Is stimulated by input from the carotid chemoreceptor.
  • Is inhibited by input from the aortic baroreceptors.
117
Q

HR is increased by all except

  • Hypoxia
  • Decreased activity of the baroreceptors
  • Fever
  • Bainbridge reflex
  • Expiration.
A

Expiration.

Inspiration causes increased venous return to the heart briefly, which causes increased atrial stretch (type B receptors in late diastole) -> ANP release -> tachycardia + drop in BP

Expiration causes the opposite -> bradycardia

118
Q

During exercise

  • Regional blood flow to the skin remains unchanged
  • Diastolic pressures tend to rise more than systolic pressure.
  • O2 consumption of skeletal muscle usually triples.
  • Blood flow to the brain increases.
  • CO increases 50 fold.
A
  • Regional blood flow to the skin remains unchanged
  • Systolic increases, diastolic decreases -> incresased pulse pressure
    • ​Incresed inotropy and chronotropy + peripheral vasodilation
  • O2 consumption of skeletal muscle usually much more than triples
  • Blood flow to the brain is Constant
    • ​Blood flow to the brain should remain unchanged throughout any normal homeostatic mechanism
  • CO increasess something <50 fold.
119
Q

With respect to BP control

  • The stress relaxation mechanism is one of the immediate responses.
  • Angiotensin acts by increasing venous tone.
  • Baroreceptors are activated over the course of hours.
  • The renin angiotensin system is vital in controlling the effect of excess Na intake
  • Renal responses precede capillary fluid shifts.
A

The renin angiotensin system is vital in controlling the effect of excess Na intake

  • The stress relaxation mechanism is one of the immediate responses.
    • Stress relaxation is where the aorta or bladder etc will have a sudden increase in wall stress in response to an increase in volume, but the stress will reduce over time as the wall tension relaxe - is not an immediate response, and does not seem to respond much to pulsatile flow, but more of a contstant increase in radius/volume.
  • Angiotensin acts by increasing arterial tone.
  • Baroreceptors are activated over the course of seconds
    • ​provide beat to beat changes in BP - eg standing from sitting
  • Renal responses follow capillary fluid shifts.
120
Q

Oxygen debt

  • Can be measured during exercise
  • Trained athletes are able to incur a greater oxygen debt for the same level of exertion as an untrained athlete
  • Is proportional to the degree of aerobic metabolism
  • Is used to replenish phosphoylcreatine stores and replace oxygen from myoglobin
  • Can occur in severe chronic respiratory disease
A

Is used to replenish phosphoylcreatine stores and replace oxygen from myoglobin

During exercise PC donates phosphate to ADP to create ATP and is used as a short-term energy store, but must be replenished at rest

Myoglobin is a short-term oxygen store in the same fashion, and must be replenished at rest

121
Q

All of the following changes occur at birth except

  • Pulmonary vascular resistance falls to less than 20%
  • Increase in peripheral resistance
  • Closure of the foramen ovale within a few hours
  • Closure of the ductus arteriosus within a few hours
  • Negative intrapleural pressure of -30 to -50 mmHg in the first few gasps
A

Increase in peripheral resistance

Not specifically mentioned in Moores. Everything else is definitely correct, but foramen ovale - closes as soon as LA pressure > RA (minutes), so this is the only other possibility.

122
Q

HR is accelerated by

  • Grief
  • Increased Baroreceptor activity
  • Increased atrial stretch receptor activity
  • Expiration
  • A direct effect on angiotensin
A

Increased atrial stretch receptor activity

To compensate for increased pre-load, HR will increase as BP drops

123
Q

Which is not correct about the reflex mechanisms acting on the circulation

  • The baroreceptors in the carotid bodies are stimulated when the BP increases.
  • The Bainbridge reflex causes increases in HR
  • The Cushing reflex is a special CNS ischaemic response resulting from raised ICP
  • The maximum firing per change in pressure of the carotid baroreceptors occurs at a MAP of 90mmHg
  • IX is involved in the Baroreceptor reflex.
A

The baroreceptors in the carotid sinus are stimulated when the BP increases.

Aortic and carotid bodies are involved in chemoreceptor response. Aortic have and carotid sinus have baroreceptors

  • The Bainbridge reflex causes increases in HR
    • ​Bainbridge reflex is an increased HR in response to increase atrial filling / pre-load
  • The Cushing reflex is a special CNS ischaemic response resulting from raised ICP
    • Pathological process - ischaemia of RVLM causes peripheral hypertension to try and restore blood flow. This causes a bradycardia due to baroreceptor response.
  • The maximum firing per change in pressure of the carotid baroreceptors occurs at a MAP of 90mmHg.
    • At higher MAPs, the receptors are firing nearly constantly, so the change between systole and diastole is less. At low MAPs, there is very little firing, so again the change is very little
  • IX is involved in the Baroreceptor reflex.
    • Carries carotid sinus afferents
124
Q

when the X fibres to nodal tissue is stimulated

  • the membrane becomes hyperpolarized
  • the slope of the prepotential is decreased
  • ACh decreases conductance to Ca via muscarinic receptors
  • ACh increases the permeability of nodal tissues to K via muscarinic receptors
  • All of the above are true
A

All of the above are true

Vagal nerve endings have ACh release -> M2 stimulation (Gi -> decreased cAMP) -> increased K flux -> hyperpolarisation of the cell membrane

also M2 -> Reduced Ca flux causing a reduced slope of the prepotential, slowing the HR

125
Q

HR is accelerated by

  • Decreased activity of the baroreceptors in the left ventricle.
  • Increased activity of baroreceptors in the pulmonary circulation
  • Increased intracranial pressure
  • Expiration
  • Increased activity of the baroreceptors in the arteries
A

Decreased activity of the baroreceptors in the left ventricle.

Ventricular distension results in increased ventricular receptor firing which causes reflex bradycardia and hypotension (comparable to a baroreceptor reflex), so the opposite is also true.

The rest cause bradycardia

126
Q

arteriolar constriction is caused by

  • kinins
  • decreased NA discharge
  • circulating angiotensin I
  • circulating Na/K ATPase inhibitor
  • decreased pH
A

circulating Na/K ATPase inhibitor

Whatever that is

(Reduced Na/K activity -> increased K outside of cells -> lowered membrane potential -> increased excitability/tone)

127
Q

factors affecting (stimulating?) the vasomotor area in the medulla are

  • inhibitory inputs from carotid and aortic chemoreceptors.
  • direct stimulation by CO2
  • excitatory inputs from the carotid, aortic and cardiopulmonary baroreceptors.
  • excitatory inputs from the lungs.
  • inhibitory inputs from cortex via the hypothalamus.
A

direct stimulation by CO2

This is the response elicited in the Cushing Reflex -> rise in BP

All others listed cause an inhibiton of the vasomotor area (ie act to reduce BP)

  • inhibitory inputs from carotid and aortic chemoreceptors.
    • Seem to only have excitatory output in response to hypoxia or hypercapnia (or acidosis) -> vagal output but multiple pathways including respiration -> tachypnoea and catecholamine release through other hypoxic mechanisms
      • (Nicks answer in contrast to my understanding): Would inhibit vasomotor ares - inhibition from receptors occurs due to low CO2 or high O2
  • excitatory inputs from the carotid, aortic and cardiopulmonary baroreceptors.
    • Would inhibit vasomotor area - fire in response to high BP
  • excitatory inputs from the lungs.
    • Receptors from the lungs fire during inspiration, travel via IX and inhibit RVLM discharge
  • inhibitory inputs from cortex via the hypothalamus - wrong
    • Inputs from higher centres are excitatory
128
Q

regarding cardiovascular regulatory mechanisms, which is false

  • decreases in O2 tensions and increases in local CO2 concentrations lead to coronary artery dilation
  • circulating vasoconstrictors hormones include angiotensin II and aldosterone.
  • vasomotor control is mediated by the Baroreceptor reflex
  • increased Baroreceptor activation slows down the HR
  • the vasomotor area is stimulated by hypoxia and pCO2
A

circulating vasoconstrictors hormones include angiotensin II, noradrenaline, vasopressin, urotensin-II

Aldosterone is not a vasoconstrictor

129
Q

After 1L of blood is lost

  • The haematocrit increases immediately.
  • Iron reabsorption is not increased
  • Equals loss of 35% plasma volume.
  • Plasma protein synthesis is not increased.
A

Iron reabsorption is not increased

Dont know exactly, will probably come up in later study but likely something to do with iron not being reabsorbed in the first place

  • The haematocrit decreases but not immediately
    • ​Need time for extravascular fluid to diffuse back into the vascular space and dilute the haematocrit before it drops
  • Equals loss of 35% plasma volume.
    • Mathematically ~28% of plasma volume is approx. 1L of fluid (3.5L plasma in a 70kg person) however the response to this would be different
  • Plasma protein synthesis is increased.
130
Q

Regarding CO in exercise

  • It can increase up to 200%
  • It can increase up to 500%
  • It can increase up to 700%
  • It can increase up to 300%
  • It can increase up to 400%
A

It can increase up to 700%

ie 7x resting output

131
Q

In exercise in a fit healthy young male

  • SV increases less than 200%
  • SV increases more than 300%
  • SV increases more than 400%
  • SV increases more than 700%
A

SV increases less than 200%

Most of increase in CO is due to increase in HR apparently

132
Q

which of the following is not part of the compensatory system activated by haemorrhage

  • increased EPO secretion
  • increased insulin secretion
  • increased ADH secretion
  • increased glucocorticoid secretion
  • increased renin secretion
A

increased insulin secretion

Others all cause increase in RBC production (EPO) or maintenence of blood volume / reduce urine output

133
Q

Which of the following statements regarding cardiovascular regulatory mechanisms is true

  • The Cushing reflex is characterized by hypertension and tachycardia as cerebral interstitial fluid accumulates when raised intracranial pressure compromises cerebral blood flow.
  • Increased Baroreceptor discharge from the carotid sinus and aorta elevates BP and HR via increased sympathetic discharge.
  • NA, A, Angiotensin II and ADH are all hormones responsible for local tissue blood flow autoregulation.
  • In general, tissue blood flow is regulated according to the needs of the tissue, CO is regulated according to the sum of tissue blood flow and BP is regulated independently of either local blood flow or CO
  • Increased CVP produces the same sympathetic response from atrial stretch receptors as elevated BP produces from carotid sinus baroreceptors.
A

In general, tissue blood flow is regulated according to the needs of the tissue, CO is regulated according to the sum of tissue blood flow and BP is regulated independently of either local blood flow or CO

  • The Cushing reflex is characterized by hypertension and bradycardia as cerebral interstitial fluid accumulates when raised intracranial pressure compromises cerebral blood flow.
  • Increased Baroreceptor discharge from the carotid sinus and aorta will result in decreased SNA, HR and BP (as it fires in response to elevated BP)
  • NA, A, Angiotensin II and ADH are all circulating hormones or neurotransmitters, and none are involved in local autoregulation. Local autoregulation involves metabolites and NO
  • Increased CVP produces differing sympathetic response from atrial stretch receptors compared to the response elevated BP produces from carotid sinus baroreceptors.
    • Discharge of atrial stretch receptors results in vasodilation and a fall in BP but an increase in HR
    • Baroreceptors cause a bradycardia and reduction in BP
134
Q

increased Baroreceptor discharge

  • inhibits GABA secreting neurons in the medulla.
  • inhibits X stimulation of the heart
  • inhibits tonic discharge of vasoconstrictor nerves
  • is inversely proportional to pressure change
  • passes via efferent nerves in IX and X nn.
A

inhibits tonic discharge of vasoconstrictor nerves

  • stimulates GABA secreting neurons in the medulla to suppress the RVLM
  • Stimulates X stimulation of the heart -> bradycardia
  • is inversely proportional to pressure change
  • passes via afferent nerves in IX and X nn.
135
Q

Increased Baroreceptor discharge acts via the medulla to

  • Increase HR
  • Increase SV
  • Increase vessel diameter
  • Increase BP
  • Increase renin
A

Increase vessel diameter

136
Q

During exercise

  • Regional blood flow to the skin remains unchanged
  • Diastolic pressures tend to rise more than systolic pressure
  • O2 consumption of skeletal muscle usually triples
  • Blood flow to the brain increases
  • CO increases 50 fold
A

Regional blood flow to the skin remains unchanged

137
Q

A subject is injected with a substance that caused: increase in HR, no change in BP, did not impair ejaculation, decreased sweating, papillary dilation – it was most likely:

  • Nicotinic antagonist
  • Nicotinic agonist
  • α blocker
  • muscarinic antagonist
A

muscarinic antagonist

M2 receptors on heart cause bradycardia when stimulated (vagal nerve is main driver of HR through inhibiton)

M receptors on sweat glands are the only acetlycholine receptors in the sympathetic nervous system

All vasomotor tone is controlled by sympathetic system

Nicotinic receptors are not found in heart or sweat glands

alpha blocker could cause tachycardia via peripheral vasodilation but would impair ejaculation and affect BP

138
Q

if the autonomic nerve supply is removed from the heart

  • HR 150 bpm.
  • HR 40 bpm
  • Decreased contractility
A

Decreased contractility

Denervated hearts run at 100bpm.

At rest:

  • Vagal tone predominates in the heart, lowering the HR. If vagal tone is cut, HR is about 150bpm. If there is loss of all innervation, HR is about 100bpm.
  • Sympathetic tone increases contractility and constricts blood vessels - if nerves are cut they vasodilate (Parasympathetic nerves have no effect on vasculature or resistence)

If dennervated:

  • Loss of parasympathetic dampening causes the HR to increase to about 100, whilst the loss of sympathetic stimulation will reduce contractility (ie at rest PNS is reducing HR, whilst SNS is increasing contractility from ‘baseline’)
139
Q

which of the following have a specific β effect on smooth muscle contraction

  • adrenaline
  • noradrenaline
  • isoprenaline
A

isoprenaline

Is a non-selective beta-agonist -> treat bradycardia

Norad and adrenaline have alpha effects

140
Q

Which of the following is a compensatory response to shock

  • Decreased ADH
  • Increased thoracic pumping
A

Increased thoracic pumping

Shock -> increased ADH as there is a desire to maintain the bodys fluid, not loose it in urine

141
Q

Regarding the rapid control of blood pressure all of the following are true EXCEPT:

  • Noradrenaline and adrenaline are secreted in response to a fall in blood pressure
  • Vasopressin is released from the supraoptic nuclei
  • The reninangiotensin system is brought into play
  • The kidneys bring the blood pressure to near normal
  • The baroreceptor mechanism operates best during fluctuations of blood pressure
A

Vasopressin is released from the supraoptic nuclei –

ADH or vasopressin is made in the cell bodies in the SON, but the axons project to the posterior pituitary for release of the hormone.

  • Noradrenaline and adrenaline are secreted in response to a fall in blood pressure
  • The reninangiotensin system is brought into play
  • The kidneys bring the blood pressure to near normal
    • via the atrial reflexes (the volume reflex) -> dilatation of afferent arteriole -> rise in GFR. Also signals from atria to hypothalamus ->ADH causing reduced reabsorption of fluid in the renal tubule, increasing urine output and reducing blood volume. Also, release of atrialnatriuretic peptide increases urine output and thus reduces blood volume.
  • The baroreceptor mechanism operates best during fluctuations of blood pressure
142
Q

Which of the following pairs are correctly matched?

  • Bradykinin – vasoconstriction
  • Vasopressin – vasodilation
  • Noradrenaline – vasoconstriction
  • Nitric oxide – vasoconstriction
  • Prostacyclin – vasoconstriction
A

Noradrenaline – vasoconstriction

143
Q

regarding factors which affect arteriolar calibre

  • kinins cause vasoconstriction
  • serotonin causes vasodilation
  • histamine causes vasoconstriction
  • lactate causes vasoconstriction
  • neuropeptide Y causes vasoconstriction
A

neuropeptide Y causes vasoconstriction

others are all opposite

144
Q

On standing the typical cardiovascular response is

  • an increase in total peripheral resistance by 75%
  • an increase in stroke volume by 10%
  • an increase in cardiac output by 50%
  • a decrease in central bloodpool by 400ml
  • a decrease intra-abdominal vascular resistance
A

a decrease in central bloodpool by 400ml

Standing causes a reduction in preload (reduced venous return/EDV) -> reduced SV -> increased HR to maintain CO (do not need to increase it - just maintain what it previously was)

  • an increase in total peripheral resistance by 40%
    • Increased peripheral SNS activity stimulates arteriolar vasoconstriction – increasing the TPR by 1:1.4 (i.e. 40%)
  • an increase in stroke volume by 10%
    • venous return will drop, thus so will preload and therefore SV. HR increases to compensate for this
  • No change in CO - just need to maintain, not increase
  • a increase in intra-abdominal vascular resistance as intraabdominal pressure will rise
145
Q

at an arterial blood pressure of 70mmHg

  • carotid sinus receptors are strongly stimulated
  • carotid body receptors are strongly stimulated
  • central nervous system ischaemia response is activated
  • both carotid body and carotid sinus receptors are strongly stimulated
  • none of the above are true
A

carotid body receptors are strongly stimulated

they will be poorly perfused and therefore activated by a reduction in PO2 (stagnant anoxia). These receptors are responsible for the Mayer Waves seen in hypotension: 20-40s fluctuations in BP as feedback is looped.

  • carotid sinus receptors are very weakly stimulated
    • they are stimulated by high pressures not low
  • central nervous system ischaemia response is not quite activated
    • Only activates <40mmHg
146
Q

Regarding changes in cardiac function during strenuous exercise

  • Oxygen usage may increase up to 10 times
  • Cardiac output it less than 6.4L/min
  • Stroke volume may double
  • A-V difference is ten times greater than at rest
  • Pulse rate is between 60 and 100 beats/min
A

Oxygen usage may increase up to 10 times

  • Cardiac output may be up to 20.9L/min
  • Stroke volume has a small range it can increase - increased inotropy but due to increased HR diastolic time shortens and thus EDV has a plateau
  • A-V difference is maybe 3-4x greater than at rest
  • Pulse rate is up to 170+bpm
147
Q

In the coronary circulation

  • Blood flow is maximal during systole.
  • 45-50% of O2 is extracted.
  • lactate is a vasodilator
  • β adrenergic receptors mediated vasoconstriction.
  • the ostia of coronary arteries are shut during systole.
A

lactate is a vasodilator

  • Blood flow is maximal during Diastole
  • 70-80% of O2 is extracted.
  • β adrenergic receptors mediated vasodilation
    • If beta receptors are blocked, noradrenaline causes vasoconstriction through alpha action, but the increased HR and inotropy brought about via beta-receptors -> increased myocardial O2 demand -> coronary vasodilation​
  • the ostia of coronary arteries are held open throughout the cardiac cycle
148
Q

1 Regarding ECG changes, which is CORRECT?

  • a) hypernatraemia is associated with low voltage complexes
  • b) the first change in hyperkalaemia is prolongation of QRS
  • c) with hypokalaemia, the resting membrane potential decreases
  • d) in hyperkalaemia, the heart stops in systole
  • e) in hypercalcaemia, myocardial contractility is enhanced
A

e) in hypercalcaemia, myocardial contractility is enhanced

  • a) hypernatraemia is associated with high voltage complexes
  • b) the first change in hyperkalaemia is peaked t-waves
  • c) with hypokalaemia, the resting membrane potential decreases
    • Need to clarify this point - hypokalaemia hyperpolarises the cell (ie more negative RMP) - Ganongs has contradictory points in the nerves and cardiology sections on this
    • Gangongs in Cardiology states that hyperkalaemia reduces the RMO
  • d) in hyperkalaemia, the heart stops in diastole
    • ​This is because as the voltage-gated sodium channels begin to close (inactivation gates) and the myocardium becomes unresponsive to stimulation (see notes for full details)
149
Q

2 Regarding jugular pressure waves:

  • a) the ‘v’ wave denotes the increased atrial pressure due to the bulging of the tricuspid valve during isovolumetric ventricular contraction
  • b) in tricuspid insufficiency, there is a giant ‘A’ wave with each ventricular systole
  • c) atrial premature beats produce an ‘A’ wave
  • d) the ‘v’ wave occurs during systole
  • e) a giant ‘C’ wave (‘cannon wave’) may be seen in complete heart block
A

c) atrial premature beats produce an ‘A’ wave

  • a) the ‘C’ wave denotes the increased atrial pressure due to the bulging of the tricuspid valve during isovolumetric ventricular contraction
    • A=atrial contraction, V=valve opening, C=contraction of ventricles causing AV valve to bulge
  • b) in tricuspid insufficiency, there is a giant ‘C’ wave with each ventricular systole
    • Presumably C as there will be backflow during ventricular systole
  • d) the ‘v’ wave occurs during diastole
    • ​V=AV valve opening at beginning of diastole
  • e) a giant ‘A’ wave (‘cannon wave’) may be seen in complete heart block
    • Occurs when the atria contract against a closed AV valve
150
Q

3 What factor does not alter cardiac output?

  • a) standing up
  • b) sleeping
  • c) eating
  • d) exercising
  • e) pregnancy
A

b) sleeping

Standing up reduce CO (reduced preload due to venous pooling)

All others increase it

151
Q

4 What is the O2 consumption of a beating heart at rest?

  • a) 2ml/100g/min
  • b) 9ml/g/min
  • c) 2ml/g/min
  • d) 2L/100g/min
  • e) 9ml/100g/min
A

e) 9ml/100g/min

152
Q

5 Regarding percentages of blood volume in the body:

  • a) the heart has 5%
  • b) the pulmonary circulation has the greatest percentage
  • c) the venous circulation has 35%
  • d) the aorta has 2%
  • e) capillaries have 20%
A

d) the aorta has 2%

  • a) the heart has 12%
  • b) the pulmonary circulation has 18%
  • c) the venous circulation has 54%
  • e) capillaries have 5%
  • Arteries 8%, arterioles 1%
153
Q
  1. What is a biological action of endothelin?
  • a) dilates vascular smoothmuscle
  • b) produces bronchodilation
  • c) increase GFR and renal blood flow
  • d) evokes positive inotropic and chronotropic effects on myocardium
  • e) inhibits gluconeogenesis
A

d) evokes positive inotropic and chronotropic effects on myocardium

Endothelin is the most potent vasoconstrictor known. I cannot find that is has direct myocardial effects, but HR and SV will need to increase to maintain CO in the context of increased PVR.

As a vasoconstrictor it should produce a reduced GFR

Cannot find information on its extra-vascular effects

  • **Prostacyclin -> platelet inhibition and vasodilation*
  • **TXA2 -> platelet activation and vasoconstriction*
154
Q
  1. What inhibits gene transcription for endothelin-1 secretion:
  • a) nitric oxide
  • b) angiotensin II
  • c) insulin
  • d) growth factors
  • e) catecholamines
A

a) nitric oxide

Is a vasodilator.

Endothelin production is managed in the way you would expect - vasodilators inhibit it, vasoconstrictors enhance it.

All others listed are either vasoconstrictors (AngII, catecholamines) or have no effect I know of (insulin, GF)

155
Q
  1. Regarding NO synthase:
  • a) it synthesises nitrous oxide from arginine
  • b) there are 2 isoforms
  • c) it is inactivated by haemoglobin
  • d) NOS-1 is activated by cytokines
  • e) NOS-2 is in endothelial cells
A

a) it synthesises nitrous oxide from arginine

As per Ganongs: ‘NO is synthesised from argenine in a reaction catalysed by NO synthase’

There are 3 isoforms

NOS 1 is in nervous system (Ca2+ induced)

NOS 2 is in macrophages and immune cells (cytokine-induced)

NOS 3 is in endothelial cells (Ca2+ induced)

They thought ‘C’ but Hb is not mentioned in Ganongs either way

156
Q
  1. What factor dilates the arterioles?
  • a) decreased local temperature
  • b) myogenic theory of autoregulation
  • c) angiotensin II
  • d) increased discharge of noradrenergic vasomotor nerves
  • e) histamine
A

e) histamine

157
Q
  1. Which is NOT a baroreceptor site?
  • a) right atria at the entrance of SVC and IVC
  • b) aortic arch
  • c) left atria at the entrance of the pulmonary veins
  • d) pulmonary circulation
  • e) carotid body
A

e) carotid body

The carotid arch is, but the carotid and aortic bodies are chemoreceptors

158
Q

Regarding cerebrospinal fluid:

  • a) the total volume of CSF is 300mL
  • b) CSF is absorbed through the choroid plexus
  • c) the average CSF pressure is 220m-CSF
  • d) CSF has a higher pH than plasma
  • e) it contains very low levels of cholesterol relative to plasma
A

e) it contains very low levels of cholesterol relative to plasma

0.2 vs 175 mg/dL

Total volume is 130ml (100ml subarachnoid, 30ml in ventricles)

It is produced in the choroid plexus and absorbed by arachnoid vili

Produced at 500ml/day

pH is slightly lower than serum

Normal pressure is 112mmCSF (measured in mmCSF as that is what is pushing up against gravity in the pressure thing for LPs)

**Note that Ganongs states that lipids freely cross the BBB, and that a lot of the bodies cholestrol is in the brain (25% in Myelin), however every other answer is clearly wrong**

159
Q

12 Which substance has equal concentrations in CSF and plasma?

  • a) Ca2+
  • b) K+
  • c) Na+
  • d) PCO2
  • e) glucose
A

c) Na+

pCO2 is higher in CSF

Ca is lower

K is lower

Glucose is lower

HCO3 is equal

160
Q

13 Which vessel has the lowest PO2?

  • a) maternal artery
  • b) maternal vein
  • c) uterine vein
  • d) umbilical vein
  • e) umbilical artery
A

e) umbilical artery

Carrying deoxygenated blood from the fetus to the uterus (the foetal pulmonary artery, as it were)

Uterine vein has 80% saturation (cf 95% equivalent in adults)

Systemic venous blood (similar to the umbilical artery) is only 26% saturated

161
Q

14 During exercise:

  • a) diastolic BP increases more than systolic BP
  • b) regional blood flow to the brain doubles
  • c) cardiac output may increase 15-fold
  • d) after exercise, BP takes longer to return to normal than heart rate
  • e) O2 consumption of skeletal muscle may increase 100-fold
A

e) O2 consumption of skeletal muscle may increase 100-fold

Brain blood flow is always constant

Diastolic has a small increase, systolic a large one (due to vasodilation of peripheral vasculature)

CO increases about ??7x

HR takes longer to normalise than BP

162
Q

15 Atrial systole:

  • a) causes a decrease in atrial pressure
  • b) causes the ‘A’ wave of the jugular pulse
  • c) causes the ‘C’ wave of the jugular pulse
  • d) causes the ‘V’ wave of the jugular pulse
  • e) causes the dicrotic notch of the aortic pulse
A

b) causes the ‘A’ wave of the jugular pulse

C=contraction of ventricle causing AV bulge

V=AV Valve opening

dicrotic notch = small plateau in arterial pressure due to closure of the aortic valve (ie it is dropping into diastole, the valve closes, and the elasticity of the aorta bumps the pressure a little bit)

Obviously atrial systole increase the atrial pressure

163
Q

16 The depolarisation of cardiac muscle cells is characterised by:

  • a) a slow depolarisation, a plateau then a rapid repolarisation
  • b) initial depolarisation due to a slow Na+ influx
  • c) repolarisation due to K+ efflux through two types of K+ channels
  • d) a plateau phase due to slowly opening Na+ channels
  • e) calcium efflux during the plateau phase
A

c) repolarisation due to K+ efflux through two types of K+ channels​

They said d (definitely wrong), c) seems closest

Phase 0 - Rapid depolarisation due to rapidly opening voltage-gated Na channels

Phase 1 - initial rapid repolarisation due to closure of voltage-gated Na channels

Phase 2 - plateau due to Ca INFLUX thruogh slow-opening voltage-gated Ca channels

Phase 3 - slow repolarisation via K efflux through ‘multiple types of potassium channels’

Phase 4 - resting RMP

164
Q

17 Regarding cardiac electrical properties:

  • a) all cardiac cells have the same resting membrane potential
  • b) cholinergic fibres act predominantly by blocking tonic sympathetic input
  • c) discharge rates of pacemaker tissue does not change significantly with
  • temperature
  • d) the bundle of HIS is not the most rapidly conducting part of the conducting system
  • e) the last parts of myocardium to depolarise normally do not include the septum
A

d) the bundle of HIS (1m/s) is not the most rapidly conducting part of the conducting system

The purkinje system is (4m/s)

  • a) all cardiac cells have the same resting membrane potential
    • Myocytes -90, pacemakers -55
  • b) cholinergic fibres act predominantly by slowing Ca influx and increasing K efflux to reduce the slope of the pre-potential (mediated via M2 receptors -> decreased cAMP)
  • c) discharge rates of pacemaker tissue can change significantly with temperature
    • Hypothermia -> bradycardia
  • e) the last parts of myocardium to depolarise are the posterobasal portions of the LV, pulmonary conus, and uppermost portion of septum
165
Q

18 Abnormalities causing ECG changes in myocardial infarction include:

  • a) delayed repolarisation early on
  • b) delayed depolarisation
  • c) increased resting membrane potential
  • d) TQ segment elevation
  • e) current flow away from the infarct
A

b) delayed depolarisation​

  1. Rapid repolarisation early with current flow away from infarct due to rapid opening of K+ channels (lasts seconds to minutes) -> STE
  2. Decreased RMP with inward current flow -> TQ depression (manifesting as STE)
    * Loss of intracellular K+ with reduced Na-K ATPase activity -> negative RMP*
  3. Delayed depolarisation with outward current flow due to infarcted fibres being unable to depolarise properly -> STE
166
Q

19 Features of the venous system include all of the following EXCEPT:

  • a) total volume is approximately 55% of the total vascular volume
  • b) compliance approximately 25 times the arterial side
  • c) total volume of venules is twice the total capillary volume
  • d) valves in the cerebral circulation
  • e) substantial venoconstriction in response to noradrenaline
A

d) valves in the cerebral circulation

167
Q

20 Arteriolar constriction is caused by:

  • a) serotonin
  • b) ANP
  • c) NO
  • d) K+
  • e) histamine
A

a) serotonin

Others all dilate (except K - unsure)

168
Q

21 Regarding the inputs into the vasomotor centre:

  • a) baroreceptors causes stimulation
  • b) chemoreceptors cause inhibition
  • c) baroreceptors provide significant input below 70mmHg mean arterial pressure
  • d) atrial stretch receptors inhibit the vasomotor centre
  • e) direct inputs include pO2
A

d) atrial stretch receptors inhibit the vasomotor centre

  • a) baroreceptors causes inhibition
  • b) chemoreceptors cause inhibition
  • c) baroreceptors provide minimal input below 70mmHg mean arterial pressure (as baroreceptors are inhibitory, so hypotension ->less firing ->more constriction)
  • e) direct inputs include pCO2
    • Responsible for the Cushing response in increased ICP
169
Q

22 CSF:

  • a) volume is about 600ml
  • b) normal pressure is 5-10cm CSF
  • c) has a higher concentration of creatinine than plasma
  • d) has a higher concentration of urea than plasma
  • e) isformedsolelyinthechoroidplexus
A

c) has a higher concentration of creatinine than plasma

1.5 vs 1.2 mg/dL

  • a) volume is about 130ml
  • b) normal pressure is 112mm CSF (range 70-180mm)
  • d) has a lower concentration of urea than plasma
    • 12 vs 15 mg/dL
  • e) about 80% is formed in the choroid plexus
170
Q

23 Regarding arrhythmias, which is TRUE?

  • a) the PR interval is shortened but the QRS normal in length in Lown Ganong Levine syndrome
  • b) with respect to the long QT syndrome, the genetic defect can occur in both Ca2+ and Na+ channels
  • c) with respect to the long QT syndrome, the genetic defect can occur in both Ca2+ and K+ channels
  • d) in atrial fibrillation, the atria beat at 200-300bpm, with the ventricles varying from 80-160/minute (irregular) depending on variable AV conduction
  • e) ventricular premature beats are never benign
A

a) the PR interval is shortened but the QRS normal in length in Lown Ganong Levine syndrome

Aberrant pathway near AV node which bypasses it but still excites the intraventricular conducting system

Long QT mutations can occur in Na or K channels

In AF the atria beat at 300-500bpm and ventricles at 80-160

SVT has atrial rates up to 220/min

Atrial flutter has trial rates 200-350/min

PVCs can be benign

171
Q

24 With regards to CSF and the blood brain barrier, which is NOT true?

  • a) the concentration of K+ in CSF is 2.9
  • b) the concentration of creatinine is approximately equal to that of plasma
  • c) the kety method utilises inhaled N2O to determine cerebral blood flow
  • d) injection of hypotonic fluids can disrupt the blood brain barrier
  • e) the chemoreceptor trigger zone for vomiting is in the area postnema
A

b) the concentration of creatinine is approximately equal to that of plasma

1.5mg/dL vs 1.2mg/dL (ie 1.25x as much in CSF)

172
Q

25 Foetal circulation, which is TRUE?

  • a) HbF has a higher affinity for O2 than HbA as it binds 2,3DPG more effectively than HbA
  • b) the sucking action of the first breath in the newborn, plus constriction of the umbilical veins, squeezes as much as 250ml blood from placenta
  • c) bradykinin dilates umbilical veins and the ductus arteriosus, while constricting the pulmonary bed
  • d) blood in the umbilical veins is believed to be about 80% saturated with O2
  • e) the placenta is a more efficient gas exchange organ than the adult lungs
A

d) blood in the umbilical veins is believed to be about 80% saturated with O2

  • a) HbF has a higher affinity for O2 than HbA as it binds 2,3DPG less effectively than HbA
  • b) the sucking action of the first breath in the newborn, plus constriction of the umbilical veins, squeezes as much as 100ml blood from placenta
  • c) bradykinin constricts umbilical veins and the ductus arteriosus, while dilating the pulmonary bed
    • Bradykinin is released from lungs during the first few breaths into the foetal circulation
  • e) the placenta is a less efficient gas exchange organ than the adult lungs - hence foetal blood is only 80% saturated in the umbilical vein
173
Q

26 Regarding the conduction system of the heart:

  • a) the right bundle branch (of HIS) divides into anterior and posterior fasicles
  • b) the AV node contains P cells
  • c) myocardial fibres have a resting membrane potential of -60mV
  • d) action potential in the SA and AV nodes are largely due to Na+ influx
  • e) there are two types of K+ channels in pacemaker tissue – transient and long acting
A

b) the AV node contains P cells

as does the SA node

  • a) the left bundle branch (of HIS) divides into anterior and posterior fasicles
  • c) myocardial fibres have a resting membrane potential of -90mV
  • d) action potential in the SA and AV nodes are largely due to Ca2+ influx
  • e) there are two types of Ca2+ channels in pacemaker tissue – transient and long acting
174
Q

27 During systole:

  • a) the peak left ventricular pressure is 160mmHg
  • b) contraction of the atria propels 70% of the ventricular filling
  • c) the period of isovolumetric ventricular contraction is 0.5sec????
  • d) the end systolic ventricular volume is about 50mL
  • e) coronary blood flow to subendocardial portions of the left ventricle occur only in systole
A

d) the end systolic ventricular volume is about 50mL

isovolumetric contraction is 0.05sec

peak pressure is about 120mmHg in LV and 25 in RV

EDV is about 130ml, SV is about 70-90ml, hence ESV is about 50ml

EF is about 70%

Atria only contribute a very small amount to ventricular filling

175
Q

28 Regarding cardiac output:

  • a) “energy of contraction is proportional to the initial length of the cardiac muscle fibre” is Fick’s Law of the heart
  • b) cardiac index is the correlation between resting cardiac output and height
  • c) sleep decreases cardiac output
  • d) basal O2 consumption by the myocardium is 2ml/g/min
  • e) standing normally decreases the length of ventricular cardiac muscle fibres
A

e) standing normally decreases the length of ventricular cardiac muscle fibres

as venous return falls -> smaller EDV

CI is CO vs BSA

Sleep has no effect on CO

basal O2 consumption is 2ml/100g/min

  • Bainbridge Reflex - increased venous return -> increased HR
  • Ficks Law - relationship of diffusion to surface area and diffusion coefficient
  • Starlings law - compares contraction strength to the initial myocyte length (aka SV to EDV)
  • Poiselles law - relationship between flow in a tube and radius/viscosity
  • Laplaces law - relationship between vessel diameter/pressure and wall tension
176
Q

29 Effects of electrolyte changes:

  • a) PR interval increases in hyperkalaemia
  • b) in hyperkalaemia, the heart stops in systole
  • c) hypercalcaemia causes prolongation of the ST segments
  • d) hypernatraemia is associated with low voltage electrocardiographic complexes
  • e) magnesium counteracts digitalis toxicity
A

e) magnesium counteracts digitalis toxicity

Magnesium suppresses digoxin-induced ventricular arrhythmias

  • a) PR interval increases in hypo-kalaemia
  • b) in hyperkalaemia, the heart stops in diastole
  • c) hypercalcaemia causes shortening of the QT segments
    • Opposite effects to potassium
  • d) hypernatraemia is associated with high voltage electrocardiographic complexes
177
Q

30 Which statement is TRUE regarding cardiac muscle?

  • a) cardiac muscle fibres are multinucleated
  • b) they are smaller than skeletal muscle fibres
  • c) Ca2+ release is triggered by membrane repolarisation
  • d) the elastic ‘Titin” protein component is greater than in skeletal muscle, adding stiffness
  • e) the amount of Ca2+ in the sarcoplasmic reticulum is decreased by catecholamine stimulation
A

b) they are smaller than skeletal muscle fibres

Skeletal muscle is multinucleated, whereas cardiomyocytes are generally mononucleated

Ca is released due to DEpolaristion

Catechols -> incresaed SR Ca

178
Q

31 Which statement regarding cardiac “work” is FALSE?

  • a) the energy applied to the blood stream is defined as kinetic plus potential
  • b) potential energy involves consideration of energy stored in elastic arterial walls and gravity
  • c) there is an exchange between kinetic and potential energy
  • d) the largest drop in energy occurs at the level of the precapillary sphincters
  • e) the higher resistance in smaller calibre vessels corresponds to greater energy losses
A

d) the largest drop in energy occurs at the level of the small arteries and arterioles.

The largest drop in pressure is at the small arteries and arterioles. I assume this is what they mean. Otherwise, who knows.

179
Q

32 Which statement about blood flow is FALSE?

  • a) cardiac output = stroke volume x heart rate
  • b) the volume of blood pumped through the lungs equals the volume entering the heart
  • c) Poiseville’s Law predicts the effects of pressure and resistance on cardiac output
  • d) the resistance of the systemic circulation is 5 to 10 times the pulmonary vascular resistance
  • e) with constant pressure, a vessel with radius ‘2X ‘ has 16 times the flow of vessel with radius ‘X’
A

b) the volume of blood pumped through the lungs equals the volume entering the heart

c) Poiseville’s Law predicts the effects of pressure and resistance on cardiac output

One of these two - they say b) is false, I cannot find anything about it.

Poiseuilles law relates flow to radius and viscosity, which would infer resistence (radius) and CO (flow) also apply.

180
Q

33 Regarding haemodynamic principles, which statement is FALSE?

  • a) viscosity of blood with haematocrit of 40 is three times that of water
  • b) ‘arterial’ blood volume is 10-15% total volume
  • c) ‘elastance’ measures a vessel’s stiffness or recoil
  • d) aging causes increased elastance and therefore decrease in resting (unstressed) arterial volume
  • e) an increase in total peripheral resistance leads to increased arterial volume and BP
A

They say d)

a) wholse blood is 3-4x as viscous as water - so likely correct
b) arteries contain 8%, aorta 2%, aterioles 1%, so b) is correct if they are including all 3 in one but that is confusing
c) Correct
d) False
e) seems false as increasing TPR (constriction) should either reduce arterial volume or have a negligible effect on it

181
Q

34 Considering conduction rates in myocardial cells, which statement is TRUE?

  • a) Perkinje fibres are subepicardial and are the largest fibres, 4-7 times the width of other fibres
  • b) Perkinje fibres are ‘fast fibres’, and can conduct a wave of depolarisation at a speed of 4m/sec
  • c) the duration of the action potential and refractory period in fast fibres is shorter than slow fibres
  • d) initial depolarisation occurs in fast fibres with a rapid influx of Ca2+ ions from the sarcoplasmic reticulum
  • e) none of the above statements are true
A

b) Perkinje fibres are ‘fast fibres’, and can conduct a wave of depolarisation at a speed of 4m/sec

182
Q

35 With respect to splanchnic circulation:

  • a) the liver is approximately 50% blood by volume
  • b) zone 3 of the hepatic acinus is well oxygenated
  • c) abdominal viscera receive at 30% cardiac output
  • d) liver receives blood from hepatic artery (1000ml/min) and hepatic vein (500ml/min)
  • e) muscular layer of intestinal wall has higher flow of mucosal layer
A

They think c) which is wrong - liver and kidneys alone are ~50% CO

I would say d) knowing nothing more than the information below.

Liver - 28% of CO (1500ml/min)

Kidneys - 23% (1260ml/min)

Brain - 14% (750ml/min)

Skin - 8%

Skeletal muscle - 16%

Heart - 5%

183
Q

36 Blood pressure:

  • a) the sounds of Korotkoff when taking blood pressure are caused by laminar flow
  • b) the diastolic pressure in resting adults correlates to the muffling of Korotkoff sound
  • c) pressures obtained by palpation of auscultation methods are usually 2-5mmHg higher
  • d) if cuff is inflated for some time, it can give falsely low BP readings
  • e) sounds of Korotkoff occur when velocity of flow through constriction exceeds critical velocity
A

e) sounds of Korotkoff occur when velocity of flow through constriction exceeds critical velocity

Turbulence is determined by Reynold formula, which essentially gives a maximum speed for laminar flow, all other factors being the same. Above this velocity, flow is turbulent

  • a) the sounds of Korotkoff when taking blood pressure are caused by turbulent flow
  • b) the diastolic pressure in resting adults correlates to the disappearance of Korotkoff sounds
    • ​correlates with muffling in adults after exercise and children
  • c) pressures obtained by palpation of auscultation methods are usually 2-5mmHg higher ???
  • d) if cuff is inflated for some time, it can give falsely low BP readings
184
Q

37 Coronary circulation:

  • a) left coronary artery has greater flow in 50% of people
  • b) thebesian veins connect arterioles to the heart chambers
  • c) cusps of the aortic valve occlude orifices of coronary arteries during LV ejection
  • d) coronary flow at rest is 250ml/min
  • e) at rest, heart extracts 50% O2 / unit of blood delivered
A

d) coronary flow at rest is 250ml/min

  • a) left coronary artery has greater flow in 10-20% of people
    • 80-90% of people are right dominant
  • b) thebesian veins connect capillaries to the heart chambers
  • c) cusps of the aortic valve never occlude orifices of coronary arteries - they are always patent
  • e) at rest, heart extracts 70-80% O2 / unit of blood delivered
185
Q

38 Regarding blood vessels:

  • a) the large diameter arteries are the major site of resistance to blood flow
  • b) true capillaries are about 5μm in diameter at the arterial end and 9μm in diameter at the venous end
  • c) the aorta wall is 1mm thick
  • d) lymphatic endothelium contains fenestrations
  • e) angiogenin inhibits angiogenesis
A

b) true capillaries are about 5μm in diameter at the arterial end and 9μm in diameter at the venous end

  • a) arterioles are the major site of resistance to blood flow
  • c) the aorta wall is 2mm thick
  • d) lymphatic endothelium does not contains fenestrations
  • e) angiogenin ?promotes angiogenesis
186
Q

39 Regarding blood flow:

  • a) turbulence is always present when ??? is more than 2,000
  • b) flow is displacement per unit time (cm/s)
  • c) velocity is proportionate to flow multiplied by the area of the conduit
  • d) the Poiseville-Hagen formula gives the relation between the flow in a long narrow tube, the viscosity of the fluid and the radius of the tube
  • e) whole blood is 7 times as viscous as water
  • f) turbulence is more frequent in polycythaemia because the viscosity of the blood is higher
A

d) the Poiseville-Hagen formula gives the relation between the flow in a long narrow tube, the viscosity of the fluid and the radius of the tube

Whole blood is 3-4x as viscous as water

187
Q

40 Regarding venous circulation:

  • a) pressure is higher in the veins compared with the venules
  • b) central venous pressure averages 6.4mmHg and fluctuates with respiration and heart action
  • c) the drop in venous pressure during expiration aids venous return
  • d) peripheral venous pressure is not affected by gravity
  • e) venous flow may be pulsitile
A

e) venous flow may be pulsitile

Varies with respiration and heart beat

  • a) pressure is higher in the venules compared with the veins (12-18mmHg vs 5.5)
  • b) central venous pressure averages 4.6mmHg and fluctuates with respiration and heart action
  • c) the drop in venous pressure during inspiration aids venous return
  • d) peripheral venous pressure is affected by gravity
188
Q

41 Which does not cause vasodilation?

  • a) decreased O2 tension
  • b) increased temperature
  • c) decreased K+
  • d) increased osmolality
  • e) adenosine
  • f) decreased pH
A

c) decreased K+

increased K causes vasodilation

189
Q

42 Regarding vasoactive substances:

  • a) endothelial cells produce new cyclo oxygen over four days
  • b) nitrous oxide synthase in immune cells is induced by increased intracellular
  • calcium concentration
  • c) NO synthase inhibition leads to a prompt rise in blood pressure
  • d) endothelin-1 is a potent vasodilator
  • e) angiotensin II inhibits secretion of endothelin-1
A

c) NO synthase inhibition leads to a prompt rise in blood pressure
* This question doesnt seem to be in Ganongs, but given NO is a vasodilator is seems reasonable that it will cause a rise in TPR if it is blocked. And all other answers are wrong.*

  • a) platelets are recycled and thus replenish their cyclo oxygen over four days
  • b) nitrous oxide synthase in immune cells is induced by cytokines (endothelial and nervous is Ca)
  • d) endothelin-1 is a potent vasoconstrictor
  • e) angiotensin II stimulates secretion of endothelin-1
190
Q

43 Heart rate is slowed by:

  • a) decreased activity of baroreceptors
  • b) inspiration
  • c) Bainbridge reflex
  • d) stimulation of pain fibres in trigenial nerve
  • e) increased activity of atrial stretch receptors
A

d) stimulation of pain fibres in trigenial nerve

Most other pains increase HR

  • a) Increased activity of baroreceptors
  • b) inspiration
    • Reduced venous pressure during inspiration -> increased venous return -> tachycardia
  • c) Bainbridge reflex
    • This is a rise in HR in response to increased venous return/atrial stretch
  • e) increased activity of atrial stretch receptors - increases via Bainbridge reflex
191
Q

44 In myocardial infarction

  • a) rapid depolarisation by Ca2+ channels is shown by ST segment elevation
  • b) resting membrane potential is increased
  • c) arrhythmias in the first 30 minutes are due to re-entry whereas after 12 hours, the arrhythmias are due to increased automaticity
  • d) after three days arrhythmias are usually due to increased automaticity
  • e) failure to progression of the R wave occurs in infarction of the posterior left ventricle
A
192
Q

45 Regarding the jugular pulse:

  • a) the ‘A’ wave occurs prior to atrial systole
  • b) the ‘C’ wave is the rise in atrial pressure produced by the bulging of the mitral valve into the atria during isovolumetric ventricular contraction
  • c) the ‘V’ wave occurs during systole
  • d) venous pressure falls in expiration
  • e) cannon waves are giant ‘A’ waves seen in complete heart block
A

e) cannon waves are giant ‘A’ waves seen in complete heart block

  • Due to the atria contracting against a closed triscupid valve*
  • b) the ‘C’ wave is the rise in atrial pressure produced by the bulging of the tricuspid valve into the atria during isovolumetric ventricular contraction
193
Q

46 Which does NOT stimulate angiogenesis?

  • a) platelet factor IV
  • b) angiogenin
  • c) tissue factor
  • d) IL-8
  • e) tumour necrosis factor α
A

a) platelet factor IV