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Medicine Sem 2 > Case 4 > Flashcards

Case 4 Flashcards

1
Q

what types of cardiac muscle is the heart composed of?

  • how do they contract compared to skeletal muscle
  • duration of contraction compared to skeletal muscle
A
  1. atrial muscle
    - contract strongly in a similar way to skeletal muscle
    - duration of contraction is longer than that of skeletal muscles
  2. ventricular muscle
    - contract strongly in a similar way to skeletal muscle
    - duration of contraction is longer than that of skeletal muscle
  3. specialised excitatory and conductive muscle fibres
    - contract weakly because they contain few contractile fibrils
    - exhibit either:
    • automatic rhythmical electrical discharge in the form of action potentials
    • conduction of the action potentials through the heart
      - in effect, these muscles provide an excitatory system that controls rhythmical beating of the heart
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2
Q

what’s a syncytium?

A

a single cells or cytoplasmic mass containing several nuclei, formed by the fusion of cells or by division of nuclei

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3
Q

what are intercalated discs?

A
  • these are cell membranes that separate individual cardiac muscle cells (cardiomyocytes) from one another
  • cardiac muscle fibres are made up of many individual cells connected in series and in parallel with one another
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4
Q

what are gap junctions? where are they in the heart? why are they important?

A

- These form at each intercalated disc.
- These are permeable “communicating” junctions that form where the cell membranes of two different cardiomyocytes fuse.
- They allow almost total free diffusion of ions.
 - Therefore, from a functional point of view, ions move with ease in the intracellular fluid along the longitudinal axes of the cardiac muscle fibres, so that action potentials travel easily from one cardiac muscle cell to the next, past the intercalated discs.
 - Thus, cardiac muscle is a syncytium of many heart muscle cells in which the cardiac cells are so interconnected that when one of these cells becomes excited, the action potential spreads to all of them, spreading from cell to cell throughout the latticework interconnections.

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5
Q

describe an action potential in terms of depolarisation and repolarisation of the membrane

A
  • The sodium-potassium pump, pumps out 3 Na+ ions for every 2 K+ ions it pumps in with the aid of ATP.
  • The sodium ions then diffuse in through the membrane and at the same time the potassium ions diffuse out of the neuron.
  • The potassium ions diffuse out of the neuron much more rapidly than the sodium ions diffuse into it.
  • This forms an electrochemical gradient across the neuron membrane.
  • The m gate, a positive voltage sensor, detects the voltage of the positive ions on the outside of the neuron membrane.
  • So as the K+ diffuse out, the increase in the positive voltage (due to the presence of Na+ and K+ ions) on the outside of the neuron is detected by the m gate.
  • Once this has reached a certain voltage, the m gate rapidly opens, and allows for the influx of the positive ions for the generation of an action potential. When the m gate is open, the channel is said to be activated.
  • In depolarisation, the ion selectivity filter, selects for the sodium ions, resulting in the influx of Na+ ions.
  • Depolarisation causes slow closing of the h gate. Upon closure of the h gate, the channel becomes inactivated.
  • In repolarisation, the m gate detects the decrease in the positive voltage on the outside of the membrane (due to a decreased amount of sodium ions).
  • The m gate opens again, but this time the potassium ions are selected for by the ion selectivity filter, and so there is an outflow of K+ ions from inside the neuron.
  • The ATP driven sodium-potassium pump brings about the resting potential again.
  • Upon reaching the resting potential, the h gate opens and the channel is reactivated.
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6
Q

describe the structure of voltage-gated ion channels and how this relates to its function

A
  • The voltage gated ion channels have 6 alpha-helical transmembrane proteins.
  • S4, the positive voltage sensor, is equivalent of the m gate.
  • S5 – S6 loop, the pore forming loop, allows for the selectivity of specific ions.
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7
Q

what is an action potential?

A

the change in electrical potential associated with the passage of an impulse along the membrane of a muscle cell or nerve cell.

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8
Q

describe action potentials in a cardiac muscle (ventricular muscle fibre)
- what is the main difference between this and skeletal muscle and what does this mean

A

Action potential in a ventricular muscle fibre averages about 105 millivolts:
 - The intracellular potential rises from a very negative value, about -85 millivolts, between beats to a slightly positive value, about +20 millivolts, during each beat.
 - After the initial spike, the membrane remains depolarized for about 0.2-0.3 seconds, exhibiting a plateau.
 - At the end of the plateau, the membrane repolarises abruptly.
 - The presence of this plateau in the action potential causes ventricular contraction to last considerably longer in cardiac muscle than in skeletal muscle.

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9
Q

what are the main phases oft the cardiac muscle action potential?

A

Phase 0 - Rapid depolarization
 Phase 1 - An initial rapid repolarization
 Phase 2 - A plateau – normal refractory period
 Phase 3 - A slow repolarization process
 Phase 4 – return to the resting membrane potential

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10
Q

explain depolarisation, repolarisation and the plateau for the action potential of the cardiac muscle

A

• Depolarization:
1. Due to Na+ influx through the rapid opening of voltage-gated sodium channels (Na+ current, INa).
2. Due to the potassium channels closing.
• Repolarisation: due to closure of the voltage-gated sodium channels and the opening of multiple types of potassium channels (K+ influx).
 Potassium channels:
 - Ito (transient outward potassium current): these channels open in phase 1 to allow an outflow of K+ ions.
 - Delayed rectifier potassium channels: IKr and IKs (rapid and slow): these open a little in phase 1 and fully in phase 3 to allow an outflow of K+ ions.
• Plateau: due to Ca2+ influx through the more slowly opening voltage-gated calcium channels (Ca2+ current, ICa). These are L-type calcium channels.

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11
Q

explain sodium channels role in action potentials

  • threshold
  • regenerative
  • conduction velocity
  • inactivation and reactivation
A
  • For depolarisation to occur the membrane potential must exceed the threshold potential.
  • Regenerative: if one area of the heart is depolarised, this may cause the adjacent areas to also become depolarised, independent of the stimulus.
  • The greater the influx of the sodium ions, the quicker (greater conduction velocity) the action potential and the greater the amplitude of the action potential.
  • Inactivation and reactivation of the sodium channels (m and h gate) leads to refractoriness (usually around 100ms) of the sodium channels.
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12
Q

what happens during the plateau of the action potential of the cardiac muscle?

A
  • At the same time, the voltage-gated calcium channels open, causing an influx of Ca2+ ions.
  • The calcium channels close at the end of 0.2-0.3 second plateau interval and the influx of calcium ions ceases.
  • The membrane permeability for potassium ions also increases rapidly; the voltage-gated potassium channels open, causing a rapid outflow of the K+ ions, returning the membrane potential to the resting potential.
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13
Q

what are the two effects of the action potential passing through the cardiac muscle?

A
  1. The T tubule action potentials act on the membranes of the longitudinal sarcoplasmic tubules to cause release of calcium ions into the muscle sarcoplasm from the sarcoplasmic reticulum, resulting in contraction.
  2. Calcium-induced calcium release:
    • The T tubule action potentials also open voltage-gated calcium channels in the membranes of the T Tubules themselves, which causes calcium ions to diffuse directly into the sarcoplasm.
    • The diffusion of calcium ions activates calcium release channels, also called ryanodine receptor channels, in the sarcoplasmic reticulum membrane of the longitudinal sarcoplasmic tubules.
    • This triggers the release of calcium ions from the sarcoplasmic reticulum into the sarcoplasm.
    • Calcium ions in the sarcoplasm then interact with troponin to initiate cross-bridge formation and contraction.
    • This is called calcium-induced calcium release.
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14
Q

what would happen without this extra calcium from the T-tubules?

A

the strength of cardiac muscle contraction would be reduced considerably

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15
Q

what does the strength of contraction of cardiac muscle depend on?

A

The strength of contraction of cardiac muscle depends to a great extent on the concentration of calcium ions in the extracellular fluids (fluid outside the cardiac cell that will flow in in the plateau stage of the action potential).

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16
Q

what happens at the end of the plateau of the cardiac action potential?

A

At the end of the plateau of the cardiac action potential, the influx of calcium ions to the interior of the muscle fibre is suddenly cut off, and the calcium ions in the sarcoplasm are rapidly pumped back out of the muscle fibres (via the Na+/Ca2+ exchanger) into both the sarcoplasmic reticulum and the T tubule–extracellular fluid space, stopping contraction or it is stored in the sarcoplasmic reticulum.

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17
Q

what do calcium ions bind to and what does this cause?

A

the Ca2+ ions bind to troponin, which holds tropomyosin in place. The calcium ions cause the troponin to change its shape. This pulls the tropomyosin away, causing the actin-myosin binding site to be exposed.

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18
Q

how long is the delay of th passage of the cardiac impulse from the atria to the ventricles? how is this coordinated? what is the purpose of this?

A

around 0.16 seconds

- This is coordinated by the atrioventricular node (AVN).
- The purpose of the delay is to allow the left atrium to finish depolarisation.
 - This allows the both atrium to contract ahead of ventricular contraction, thereby pumping blood into the ventricles before the strong ventricular contraction begins.

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19
Q

how do the atria act as primer pumps?

- what does this mean in terms of when the atria fail?

A
  • 80% of blood flows directly through the atria into the ventricles before atrial contraction.
  • Then, atrial contraction usually causes an additional 20% filling of the ventricles.
  • Therefore, the atria simply function as primer pumps that increase the ventricular pumping effectiveness as much as 20%.
  • When the atria fail to function, the difference is unlikely to be noticed unless a person exercises.
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20
Q

describe and explain the pressure changes in the atria

A

• The ‘a’ wave is caused by atrial contraction.
• The ‘c’ wave occurs when the ventricles begin to contract:
 - It is caused partly by slight backflow of blood into the atria at the onset of ventricular contraction but mainly by bulging of the A-V valves backward toward the atria because of increasing pressure in the ventricles.
• The ‘v’ wave occurs toward the end of ventricular contraction:
 - It results from slow flow of blood into the atria from the veins while the A-V valves are closed during ventricular contraction.
 - Then, when ventricular contraction is over, the A-V valves open, allowing this stored atrial blood to flow rapidly into the ventricles and causing the v wave to disappear.

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21
Q

describe how the ventricles are filled with blood?

  • preparation
  • action of being filled
A

• During systole large amounts of blood accumulate in the atria from the veins due to the closed A-V valves.
• Therefore, as soon as systole is over, the moderately increased pressures (‘v’ wave) that have developed in the atria during ventricular systole immediately push the A-V valves open and allow blood to flow rapidly into the ventricles, as shown by the rise of the left ventricular volume curve.
• This is called the period of rapid filling of the ventricles:
 - The period of rapid filling lasts for about the first third of diastole.
 - In the middle third of diastole, only a small amount of blood normally flows into the ventricles.
 - In the last third of diastole, the atria contract giving an additional 20% inflow of blood.

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22
Q

describe and explain the aortic pressure cuve

A

• When the left ventricle contracts, the ventricular pressure increases rapidly until the aortic valve opens.
• Then, after the valve opens, the pressure in the ventricle rises much less rapidly, because blood immediately flows out of the ventricle into the aorta.
• Next, at the end of systole, after the left ventricle stops ejecting blood and the aortic valve closes a so-called incisura (deep indentation) occurs in the aortic pressure curve when the aortic valve closes.
 - This is caused by a short period of backward flow of blood immediately before closure of the valve, followed by sudden cessation of the backflow.
• After the aortic valve has closed, the pressure in the aorta decreases slowly throughout diastole.

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23
Q

describe and explain the emptying of the ventricles during systole

A

• After ventricular contraction begins, the ventricular pressure rises abruptly causing the A-V valves to close.
• Then an additional period is required for the ventricle to build up sufficient pressure to push the semilunar valves open against the pressures in the aorta and pulmonary artery.
 - During this period, contraction is occurring in the ventricles, but there is no emptying.
 - This is called the period of isovolumic contraction.
• When the left ventricular pressure is raised sufficiently the pressures push the semilunar valves open.
• Immediately, blood pours out of the ventricles.
• The first third of the total duration is the period of rapid ejection with the next two thirds being the period of slow ejection.
• At the end of systole, ventricular relaxation allows the ventricular pressures to decrease rapidly.
• The aortic and pulmonary valves are snapped shut by back blow.
• For a short period, the ventricles continue to relax even though the ventricular volume does not change.
 - This is the period of isovolumic relaxation

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24
Q

what is the end-diastolic volume (EDV)?

A

amount of blood in ventricles at end of diastole (the highest volume in the ventricles)

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25
Q

what is end-systolic volume (ESV)?

A

amount of blood in ventricles at end of systole (the lowest volume in the ventricles)

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26
Q

what is ejection fraction (EF)?

A

fraction of end-diastolic volume that is ejected

(EDV-ESV)/EDV or SV/EDV

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27
Q

how can you greatly increase the stroke volume?

A

by both increasing the end-diastolic volume and decreasing the end-systolic volume

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28
Q

what is needed to cause closure of the valves of the heart?

A

The thin, filmy A-V valves require almost no backflow to cause closure, whereas the much heavier semilunar valves require rather rapid backflow for a few milliseconds.

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29
Q

what are the muscles that attach to the vanes of the AV valves called?

A

papillary muscles

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30
Q

what attaches the papillary muscles to the vanes of the AV valves?

A

chordae tendineae

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31
Q

what do the papillary muscles do?

A
  • The papillary muscles contract when the ventricular walls contract.
  • They pull the vanes of the valves inward toward the ventricles to prevent prolapse of the A-V valves.
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32
Q

how is the closure of the aortic and pulmonary artery valves different from the AV valves?

A

The high pressures in the arteries at the end of systole cause the semilunar valves to snap to the closed position, in contrast to the much softer closure of the A-V valves.

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33
Q

what is preload?

A

the preload is usually considered to be the end-diastolic pressure when the ventricle has become filled

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34
Q

what is afterload?

A

the afterload is the pressure in the artery leading from the ventricle against which the ventricle must contract

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35
Q

what are the basic means by which the volume pumped by the heart is regulated?

A
  1. Intrinsic cardiac regulation of pumping in response to changes in volume of blood flowing into the heart.
  2. Control of heart rate and strength of heart pumping by the autonomic nervous system.
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36
Q

sinus node

  • what is it
  • where is it
  • what doesn’t it contain
  • what does it connect to
A
  • The sinus node is a small, strip of specialized cardiac muscle, containing pacemaker cells.
  • Located immediately below and slightly lateral to the opening of the superior vena cava in the right atrium.
  • The fibres of this node have almost no contractile muscle filaments.
  • However, the sinus nodal fibres connect directly with the atrial muscle fibres so that any action potential that begins in the sinus node spreads immediately into the atrial muscle wall.
  • The SAN also connects to the internodal pathways.
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37
Q

pacemaker potential

  • what causes resting membrane potential
  • the pacemaker cells have a membrane potential that does what
  • what happens at the peak of each impulse
  • what happes at hyperpolarisation
  • how is the pre-potential formed again
  • what are the action potentials in the SA and AV nodes largely due to
  • what is the resting membrane potential
A

• The resting membrane potential (-55 to -60 millivolts) of pacemaker cells, like other cells, is caused by the continuous outflow of potassium ions through potassium channels.
• The pacemaker cells have a membrane potential that, after each impulse, declines to the firing level.
 - This prepotential or pacemaker potential triggers the next impulse.

• At the peak of each impulse, IK begins and brings about repolarization. (Ik = potassium current (flow of potassium ions)).
• IK then declines, and a channel that can pass both Na+ and K+ is activated.
 - Because this channel is activated following hyperpolarization, it is referred to as an “h” (or funny) channel.
• As Ih increases, the membrane begins to depolarize, forming the first part of the prepotential.
• Ca2+ channels then open.
 - These are of two types in the heart, the T (for transient) channels and the L (for long-lasting) channels:
1. The calcium current (ICa) due to opening of T channels completes the prepotential.
2. ICa due to opening of L channels produces the impulse.

  • The action potentials in the SA and AV nodes are largely due to Ca2+, with no contribution by Na+ influx.
  • The “resting membrane potential” of the sinus nodal fibre between discharges has a negativity of about -55 to -60 millivolts, in comparison with -85 to -90 millivolts for the ventricular muscle fibre.
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38
Q

what are the two types of calcium channels and what are they both involved in?

A

These are of two types in the heart, the T (for transient) channels and the L (for long-lasting) channels:

  1. The calcium current (ICa) due to opening of T channels completes the prepotential.
  2. ICa due to opening of L channels produces the impulse.
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39
Q

what are intermodal pathways?

A

specialised conduction tissues found in the atria

  • the anterior, middle and posterior intermodal pathways terminate directly in the AV node
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40
Q

how does the cardiac impulse travel through the atria?

A
  • The ends of the sinus nodal fibers connect directly with surrounding atrial muscle fibers.
  • Therefore, action potentials originating in the sinus node travel outward into these atrial muscle fibers.
  • In this way, the action potential spreads through the entire atrial muscle mass and, eventually, to the A-V node.
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41
Q

how does the velocity of conduction in the atrial muscle compare to conduction in the specialised tissue

A

its slower

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42
Q

where does the anterior interatrial band travel through?

A

through the anterior walls of the right atrium to the left atrium

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43
Q

where is the AV node located?

A

in the posterior wall of the right atrium, immediately behind the tricuspid valve

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44
Q

why does it take 0.16 seconds for the excitatory signal to reach the ventricles from the SAN?

A
  • 0.03 seconds to reach the A-V node.
  • 0.09 seconds delay in the A-V node.
  • 0.04 seconds delay in the penetrating A-V bundle.
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45
Q

what causes the slow conduction in the transitional, nodal and penetrating AV bundle fibres?

A

The slow conduction in the transitional, nodal, and penetrating A-V bundle fibers is caused mainly by diminished numbers of gap junctions between successive cells in the conducting pathways, so there is great resistance to conduction of excitatory ions from one conducting fiber to the next.

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46
Q

what causes the rapid transmission of action potentials by Purkinje fibres?

A
  • The rapid transmission of action potentials by Purkinje fibers is caused by a very high level of permeability of the gap junctions at the intercalated discs between the successive cells that make up the Purkinje fibers.
  • The Purkinje fibers also have very few myofibrils, which means that they contract little or not at all during the course of impulse transmission.
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47
Q

the atrial muscle is separated from the ventricular muscle by a continuous fibrous barrier everywhere except where?

A

at the AV bundle

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48
Q

how far do the ends of the Purkinje fibres penetrate into the muscle mass? and what do they become continuous with?

A

The ends of the Purkinje fibers penetrate about one third of the way into the muscle mass and finally become continuous with the cardiac muscle fibers (T-tubules etc).

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49
Q

once the impulse reaches the ends of the Purkinje fibres, what happens?

A

it is transmitted through the ventricular muscle mass by the ventricular muscle fibers themselves.

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50
Q

how does the cardiac muscle wrap around the heart? and what does this mean for how the cardiac impulse travels? and what does this mean for the time taken for transmission from the endocardial surface to the epicardial surface? and thus total time for transmission of cardiac impulse from initial bundle branches to last of the ventricular muscle fibres?

A
  • Once the impulse reaches the ends of the Purkinje fibers, it is transmitted through the ventricular muscle mass by the ventricular muscle fibers themselves.
  • The cardiac muscle wraps around the heart in a double spiral, with fibrous septa between the spiraling layers.
  • Therefore, the cardiac impulse does not necessarily travel directly outward toward the surface of the heart but instead angulates toward the surface along the directions of the spirals.
  • Because of this, transmission from the endocardial surface to the epicardial surface of the ventricle requires as much as another 0.03 second, approximately equal to the time required for transmission through the entire ventricular portion of the Purkinje system.
  • Thus, the total time for transmission of the cardiac impulse from the initial bundle branches to the last of the ventricular muscle fibers in the normal heart is about 0.06 second.
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51
Q

what’s the important of the Purkinje system of transmission and what would happen without it?

A
  • The Purkinje system normally ensures the cardiac impulse arrives at almost all portions of the ventricles within a narrow span of time, exciting the first ventricular muscle fibre only 0.03 to 0.06 second ahead of excitation of the last ventricular muscle fibre.
  • This causes all portions of the ventricular muscle in both ventricles to begin contracting at almost the same time and then to continue contracting for about another 0.3 second.
  • Effective pumping by the two ventricular chambers requires this synchronous type of contraction.
  • If the cardiac impulse should travel through the ventricles slowly, much of the ventricular mass would contract before contraction of the remainder, in which case the overall pumping effect would be greatly depressed.
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52
Q

what is the innervation of the cardiac muscle? and what does its distribution explain?

A

• The heart is innervated with both sympathetic and parasympathetic nerves.

• The parasympathetic nerves (the vagi) are distributed:
 - Mainly to the S-A node (right vagus nerve) and A-V node (left vagus nerve).
 - To a lesser extent to the muscle of the two atria.
 - Very little directly to the ventricular muscle.
• This explains the effect of vagal stimulation mainly to decrease heart rate rather than to decrease the strength of heart contraction.

• The sympathetic nerves, conversely, are distributed:
 - To all parts of the heart
 - With strong representation to the ventricular muscle.

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53
Q

in contrast to sympathetic activity, the parasympathetic nervous system has little effect on what?

A

contractility

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54
Q

what effect does the parasympathetic NS have on the heart? how does it have this effect?

A

Main effects are to alter the rate and rhythm of the heart:
- Cardiac slowing and reduced automaticity.
- Inhibition of A-V conduction.

These effects result from occupation of muscarinic (M2) acetylcholine receptors, which are abundant in nodal and atrial tissue but sparse in the ventricles.
- These receptors are negatively coupled to adenylate cyclase and thus reduce cAMP formation, acting to inhibit the slow Ca2+ current.
- M2 receptors also open a potassium channel.
- The resulting increase in K+ permeability produces a hyperpolarising current, slowing the heart and reducing automaticity.

Increased K+ permeability and reduced Ca2+ current both contribute to conduction block at the A-V node, where propagation depends on the Ca2+ current.

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55
Q

does the parasympathetic nervous system have an effect on coronary artery tone?

A

Coronary vessels lack cholinergic innervation; consequently, the parasympathetic nervous system has little effect on coronary artery tone.

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56
Q

what can strong vagal stimulation do? what happens and what does it cause?

A

completely block excitation by the sinus node or black transmission in the AV node

- In either case, rhythmical excitatory signals are no longer transmitted into the ventricles.
- The ventricles stop beating for 5 to 20 seconds.
- But then some small area in the Purkinje fibers, usually in the ventricular septal portion of the A-V bundle, develops a rhythm of its own.
- This phenomenon is called ventricular escape.

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57
Q

what does sympathetic stimulation cause?

A
  • Increased force of contraction
  • Increased heart rate
  • Faster repolarisation and restoration of function following generalised cardiac depolarisation
  • Increased rate of sinus node discharge
58
Q

how does sympathetic stimulation cause these effects?

A

Stimulation of these receptors enhances Ca2+ influx in the myocyte and thereby strengthens the force of contraction.
- Binding of catecholamines (adrenaline and noradrenaline) to the myocyte βl-adrenergic receptor activates membrane-bound adenylate kinases.
- These enzymes enhance production of cAMP that activates intracellular protein kinases, which in turn phosphorylate cellular proteins, including L-type calcium channels within the cell membrane.
- This causes an increased influx of Ca2+ ions therefore more Ca2+ ions are available for muscular contraction.
Stimulation of these receptors also enhances myocyte relaxation, so that it is ready for the next contraction more quickly.

59
Q

how does sympathetic stimulation of these B1-adrenergic receptors stimulate myocyte relaxation?

A

• The return of calcium from the sarcoplasm to the sarcoplasmic reticulum is regulated by phospholamban.
- In its dephosphorylated state, phospholamban inhibits Ca2+ uptake by the SR ATPase pump.
- βl-adrenergic activation of protein kinase phosphorylates phospholamban.
- This causes greater uptake of Ca2+ ions by the SR, promoting myocyte relaxation.
• The increased cAMP activity also results in phosphorylation of troponin I, an action that inhibits actin–myosin interaction, and further enhances myocyte relaxation.

60
Q

what does hypertrophy of the heart cause?

A

increase cardiac output

61
Q

what’s the relationship between total peripheral resistance and cardiac output? equation.

A

an increase in total peripheral resistance decreases cardiac output and vice versa

cardiac output = arterial pressure / total peripheral resistance

62
Q

how does arterial pressure and total peripheral pressure change during exercise? and how does this affect cardiac output?

A
  • During exercise, body metabolism increases.
  • This causes muscle arterioles to relax to allow adequate oxygen + nutrients.
  • This greatly decreases total peripheral resistance, which usually would decrease arterial pressure as well.
  • Nervous system immediately compensates, autonomic signals cause large vein constriction, increased heart rate, and increased contractibility.
  • All these changes acting together increase the arterial pressure above normal, which in turn forces still more blood flow through the active muscles.
  • During exercise, the nervous system goes even further, providing additional signals to raise the arterial pressure even above normal, which serves to increase the cardiac output.
63
Q

what is cardiac shock?

A

when the cardiac output falls so low that the tissues throughout the body begin to suffer nutritional deficiency

64
Q

how does intrapleural pressure affect cardiac output? what is normal intrapleural pressure?

A
  • The normal intrapleural pressure is -4 mm Hg.
  • A rise in intrapleural pressure, to -2 mm Hg, shifts the entire cardiac output curve (right atrial pressure against cardiac output) to the right by the same amount.
  • This shift occurs because to fill the cardiac chambers with blood requires an extra 2 mm Hg right atrial pressure to overcome the increased pressure on the outside of the heart.
65
Q

what are some factors that can alter the external pressure on the heart and thereby shift the cardiac output curve?

A
  1. Cyclical changes of intrapleural pressure during respiration
  2. Breathing against a negative pressure, which shifts the curve to the left
  3. Positive pressure breathing, which shifts the curve to the right.
  4. Opening the thoracic cage, which increases the intrapleural pressure to 0 mm Hg and shifts the cardiac output curve to the right 4 mm Hg.
  5. Cardiac tamponade, which means accumulation of a large quantity of fluid in the pericardial cavity around the heart with resultant increase in external cardiac pressure and shifting of the curve to the right.
66
Q

how would a hypereffectvie heart and increased intrapleural pressure affect the curve?

A
  • increased maximum level of cardiac output

- curve shifted to right

67
Q

what are the three principal factors that affect venous return to the heart?

A
  1. Right atrial pressure - which exerts a backward force on the veins to impede flow of blood from the veins into the right atrium
  2. Systemic filling pressure
  3. Resistance to venous return
68
Q

what is mean systemic filling pressure? what causes an increase in systemic filling pressure?

A

the pressure measured everywhere in the systemic circulation after blood flow has been stopped

  • When the blood flow stops, the pressures everywhere in the circulation become equal.
  • This equilibrated pressure level is called the mean circulatory filling pressure.
  • The greater the volume of blood in the circulation, the greater is the mean circulatory filling pressure because extra blood volume stretches the walls of the vasculature.
  • Strong sympathetic activity constricts systemic vessels, as well as the chambers of the heart, increasing mean circulatory filling pressure.
  • Strong inhibition of the sympathetic system relaxes the mean circulatory filling pressure.
69
Q

what does the normal venous return curve tell you? (right atrial pressure against venous return)

A
  • This curve showreatments that an increase in the right atrial pressure causes the backward force of the rising atrial pressure on the veins of the systemic circulation decreases venous return of blood to the heart.
  • Arterial pressures and the venous pressures come to equilibrium when all flow in the systemic circulation ceases at a pressure of 7 mm Hg, which, by definition, is the mean systemic filling pressure (Psf).
  • When the right atrial pressure falls below zero - further increase in venous return almost ceases.
70
Q

how does an increase in mean systemic filling pressure affect the venous return curve?

A

The greater the mean systemic filling pressure, the more the venous return curve shifts upward and to the right.

71
Q

when does venous return become zero? and what does this mean in terms of highest level to which the right atrial pressure can rise?

A

When the right atrial pressure rises to equal the mean systemic filling pressure, venous return becomes zero at all levels of resistance to venous return because when there is no pressure gradient to cause flow of blood, it makes no difference what the resistance is in the circulation; the flow is still be zero.

Therefore, the highest level to which the right atrial pressure can rise, is equal to the mean systemic filling pressure.

72
Q

where does most of the resistance to venus return occur?

A

Most of the resistance to venous return occurs in the veins, although some occurs in the arterioles and small arteries as well

73
Q

how can venous return be calculated?

A

(Psf (mean systemic filling pressure) - PRA (right atrial pressure)) / RVR (resistance to venous return)

74
Q

what’s the effect of increased blood volume on cardiac output?

A

- Increases the filling of the system, causing the mean systemic filling pressure (Psf) to increase, which shifts the venous return curve to the right.
- Distends the blood vessels, thus reducing their resistance and thereby reducing the resistance to venous return, which moves the curve upward.

75
Q

why does the greatly increased cardiac output caused by increased blood volume last only minutes?

A

because several compensatory effects immediately begin to occur:

  1. The increased cardiac output increases the capillary pressure so that fluid begins to transude out of the capillaries into the tissues, thereby returning the blood volume toward normal.
  2. The increased pressure in the veins causes the veins to continue distending gradually by the mechanism called stress-relaxation, especially causing the venous blood reservoirs, such as the liver and spleen, to distend, thus reducing the mean systemic pressure.
  3. The excess blood flow through the peripheral tissues causes autoregulatory increase in the peripheral vascular resistance, thus increasing the resistance to venous return.
  • These factors cause the mean systemic filling pressure to return back toward normal and the resistance vessels of the systemic circulation to constrict.
  • Therefore, gradually, the cardiac output returns to almost normal.
76
Q

what is heart failure?

A

a complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump to support a physiological circulation

a state that develops when the heart fails to maintain an adequate cardiac output to meet the demands of the body

77
Q

what are the effects of heart failure?

A
  • reduced cardiac output

- damming of blood in the veins, resulting in increased venous pressure

78
Q

how much blood does each ventricle eject approximately?

A
  • 70mL of blood/beat
    = 4,200 ml/min = cardiac output

the cardiac output averages between 4-8 L/min upon exertion

79
Q

what’s the pathophysiology of heart failure? - causes

A

Failure of the pump:
- Damaged muscle contracts or relaxes weakly or inadequately.
 - E.g. metabolic (diabetes), myocardial infarction, infection (viral), drugs (recreational or prescribed), endocrine (hypo/hyperthyroidism), vitamin deficiency

An obstruction to flow in heart:
- This overworks the chamber behind obstruction.
- E.g. stenosis of valves, cor pulmonale.

Regurgitation flow:
- Some of the output from each contraction is refluxed back—volume workload to ventricles.
- E.g. leaky valves.

Disorders of cardiac conduction

Disruption of the continuity of the circulatory system.
 E.g. atheromas or thrombus

80
Q

what are adaptive mechanisms to compensate for damage to the heart?

A
  1. Frank-Starling Mechanism
  2. Myocardial Structural Change (remodelling)
  3. Activation of neuro-humoral system
81
Q

describe the frank-starling mechanism

A

- States that the stroke volume increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant.
- The increased volume of blood stretches the ventricular wall, increasing functional cross-bridge formation within the sarcomeres, causing cardiac muscle to contract more forcefully, thus enhancing contractility.
- To increase the end-diastolic volume and so the stoke volume (and so the cardiac output), there is increased venous return (in many ways listed as part of other adaptive mechanisms below) to compensate for the initial decreased cardiac output.

82
Q

describe myocardial structural change (remodelling)

A

- Increase in the muscle mass (hypertrophy) with or without cardiac chamber dilatation.
- The collective molecular, cellular, and structural changes that occur as a response to injury or changes in loading conditions are called ventricular remodelling.
- This can lead to the heart being over compensated, resulting in an insufficient pump.

  • normal
  • concentric hypertrophy
  • eccentric hypertrophy
83
Q

describe the activation of neuro-humoral system as compensation

A
  • Activation of the sympathetic nervous system: acute (next page).
  • Renin-angiotensin-aldosterone system: chronic (case 6 notes).
  • Angiotensin II causes an increase in blood pressure through increasing the venous return and so increasing the cardiac output.
84
Q

describe the compensation for acute cardiac failure by sympathetic nervous reflexes

A

• This occurs in the first 30 seconds to 1 minute after damage to the heart.
• When the cardiac output falls, the sympathetic nervous system is strongly stimulated and the parasympathetic signals weaken.
• Compensation for Acute Cardiac Failure by Sympathetic Nervous Reflexes
1. Sympathetic stimulation strengthens the damaged musculature:
 The heart becomes a stronger pump as a result.
2. Sympathetic stimulation also increases venous return to the heart:
 The damaged heart receives more blood than usual, raising the right atrial pressure further, helping the heart pump larger quantities of blood.

85
Q

describe the chronic compensations for cardiac failure by humoral mechanisms

A

• This occurs after the first few minutes of the muscular damage.
• This is characterised by:
1. Retention of fluid by the kidneys (Angiotensin II pathway):
 This increases the blood volume.
 The urine output remains below normal as long as the cardiac output and arterial pressure remain significantly less than normal.
 The increased blood volume increases venous return in two ways:
o Increases the systemic filling pressure, which increases the pressure gradient for causing venous blood flow toward the heart.
o It distends (swells) the veins, which reduces the venous resistance and allows even more ease of flow of blood to the heart.
 If the heart isn’t too greatly damaged, an increase in the venous return can fully compensate for the heart’s diminished pumping ability and return the cardiac output to nearly normal.

 In severe heart damage, the blood flow to the kidneys is impaired so as to prevent excretion of salts.
o This leads to further fluid retention.
o This is no longer beneficial.
 Severe fluid retention can have serious physiological consequences:
o Increasing workload on the heart.
o Overstretching of the heart, weakening the heart.
o Filtration of fluid into the lungs, causing pulmonary oedema and consequent deoxygenation of the blood.
o Peripheral oedema.
2. Varying degrees of recovery of the heart itself over a period of weeks to months.

86
Q

what is compensated heart failure?

A
  • The final state is called compensated heart failure.
  • Any attempt to perform heavy exercise usually causes immediate return of the symptoms of acute failure because the heart is not able to increase its pumping capacity to the levels required for the exercise.
  • Therefore, it is said that the cardiac reserve is reduced in compensated heart failure.
87
Q

what is decompensated heart failure?

A
  • This occurs in very severe cases.
  • The heart is severely damaged and no amount of compensation, either by sympathetic nervous reflexes or by fluid retention, can make the excessively weakened heart pump a normal cardiac output.
  • As a consequence, the cardiac output cannot rise high enough to make the kidneys excrete normal quantities of fluid.
  • Therefore, fluid continues to be retained, the person develops more and more oedema, and this state of events eventually leads to death.
  • This is called decompensated heart failure.
88
Q

left-sided heart failure

  • causes
  • symptoms
  • what happens
A

The effects of left-sided HF result from:
- Congestion of the pulmonary circulation.
- Stasis of blood in the left-sided chambers.
- Hypoperfusion of tissues leading to organ dysfunction.

Symptoms are often related to pulmonary congestion and pulmonary oedema:
- Cough and dyspnea, initially with exertion and later at rest.
- Worsening pulmonary oedema may lead to orthopnea, requiring the patient to sleep in an upright position; or paroxysmal nocturnal dyspnea, a form of dyspnea usually occurring at night that is so severe that it induces a feeling of suffocation.
- Particularly in the setting of atrial fibrillation, stasis greatly increases the risk of thrombosis and thomboembolic stroke.

Decreased cardiac output causes a reduction in renal perfusion, which leads to the activation of the renin-angiotensin-aldosterone system.
- This causes increased retention of water, leading to further pulmonary oedema as well as peripheral oedema.

89
Q

right-sided heart failure

  • most common cause
  • often to referred to as what
  • common feature of disorders that cause it
  • organs predominantly affected
A

• Most commonly, right-sided heart failure is caused by left-sided heart failure.
• Pure right-sided heart failure is infrequent and usually occurs in patients with any one of a variety of disorders affecting the lungs; hence, it is often referred to as cor pulmonale.
• The common feature of these diverse disorders is pulmonary hypertension, which results in hypertrophy and dilation of the right side of the heart.
• The clinical features of isolated right-sided heart failure are those related to venous congestion, and include hepatosplenomegaly and peripheral oedema.
 Organs that are prominently affected in right-sided heart failure include the kidney and the brain.

90
Q

how is heart failure defined by New York Heart Association (NYHA)?

A

 NYHA 1: No symptoms and no limitation in ordinary physical activity.
 NYHA 2: Mild symptoms and slight limitation during ordinary activity.
 NYHA 3: Marked limitation in activity due to symptoms, even during less-than-ordinary activity.
 NYHA 4: Severe limitations. Experiences symptoms even while at rest.

91
Q

what are the signs of heart failure?

A 
- Pulmonary oedema /pulmonary effusion
- Raised JVC
- Pitting peripheral oedema
- Ascites (fluid in the peritoneal cavity causing swelling)
- Tachycardia
- S3 Gallop
92
Q

what are the investigations for heart failure?

A

Bloods:
- Full blood count
- Glucose: test for diabetes

Brain Natriuretic Peptide (BNP):
- 32 amino acid polypeptide secreted by the ventricles of the heart in response to excessive stretching of heart muscle cells.
- Normal levels rule out heart failure.
- Provides prognostic information, i.e. high levels predict worse outcomes

Chest X-ray:
- Cardiomegaly (enlarged heart)
- Pleural effusion
- Pulmonary oedema

Troponin T test:
- Measures the concentration of cardiac-specific troponin in the blood.
- Troponin is found in skeletal and cardiac muscle fibres and helps them contract.
- There are three forms of troponin: C, I and T.
- Cardiac I and T are different from the troponin I and T found in skeletal muscle that they can be specifically tested for.
- These types of troponin are normally present in very small quantities in the blood.
- When there is damage to heart muscle cells, cardiac troponin I and T are released into circulation.
- These can be detected 4 hours – 14 days after heart muscle damage.

Echocardiography:
- LV eject fraction

ECG
- Atrial fibrillation/arrhythmias
- Presence of old aetiologies

93
Q

drugs to treat heart failure?

A
  • diuretics
  • ACE inhibitors
  • beta-blockers
  • aldosterone receptor antagonists
  • devices (CRT(cardiac resynchronisation therapy)/ICD)
94
Q

what is a frequent cause of death in heart failure?

A

acute pulmonary oedema occurring in patients who have already had chronic heart failure

95
Q

what is acute pulmonary oedema believed to result from?

A

The acute pulmonary oedema is believed to result from the following vicious circle:

  1. A temporarily increased load on the already weak left ventricle initiates the vicious circle.
  2. Because of limited pumping capacity of the left heart, blood begins to dam up in the lungs.
  3. The increased blood in the lungs elevates the pulmonary capillary pressure, and a small amount of fluid begins to transude into the lung tissues and alveoli.
  4. The increased fluid in the lungs diminishes the degree of oxygenation of the blood.
  5. The decreased oxygen in the blood further weakens the heart and also weakens the arterioles everywhere in the body, thus causing peripheral vasodilation.
  6. The peripheral vasodilation increases venous return of blood from the peripheral circulation.
  7. The increased venous return further increases the damming of the blood in the lungs, leading to still more transudation of fluid, more arterial oxygen desaturation, more venous return, and so forth.
  8. Thus, a vicious circle has been established.
96
Q

why does acute cardiac failure almost never cause immediate development of peripheral oedema?

A

• However, either left or right heart failure is very slow to cause Peripheral Oedema.
• When a previously healthy heart acutely fails as a pump:
- The aortic pressure falls and the right atrial pressure rises.
- As the cardiac output approaches zero, these the aortic pressure and the right atrial pressure approach each other at an equilibrium.
- Capillary pressure also falls from its normal value to the new equilibrium pressure.
• Thus, severe acute cardiac failure often causes a fall in peripheral capillary pressure rather than a rise.
• Therefore, acute cardiac failure almost never causes immediate development of Peripheral Oedema.

97
Q

why does peripheral oedema begin to occur after the first day or so of overall heart failure?

A

principally due to fluid retention of the kidneys:

  1. The retention of fluid increases the mean systemic filling pressure, resulting in increased tendency for blood to return to the heart.
  2. This elevates the right atrial pressure to a still higher value and returns the arterial pressure back toward normal.
  3. Therefore, the capillary pressure now also rises markedly, thus causing loss of fluid into the tissues and development of severe oedema.
98
Q

what is rheumatic fever?

A

Rheumatic fever is an inflammatory disease that occurs in children and young adults as a result of infection with group A streptococcal pharyngitis.

99
Q

what does rheumatic fever affect?

A

 Heart: Autoimmune reaction against self-antigens in the heart.
 Skin: Skin rashes.
 Joints: Swollen, tender joints.
 Central Nervous System: Severe malaise and Fever.

100
Q

what is the primary cause of mitral regurgitation?

A

Rheumatic disease is the principal cause in countries where rheumatic fever is common but elsewhere, including in the UK, other causes are more important.

101
Q

what does regurgitation into the left atrium cause? and what happens with acute mitral regurgitation? what does this mean for the left atrial pressure waves? and what is caused?

A

Regurgitation into the left atrium produces left atrial dilatation but little increase in left atrial pressure if the regurgitation is long-standing, as the regurgitant flow is accommodated by the large left atrium.

With acute mitral regurgitation the normal compliance of the left atrium does not allow much dilatation and the left atrial pressure rises.

Thus, in acute mitral regurgitation the left atrial ‘v’ wave is greatly increased and pulmonary venous pressure rises to produce pulmonary oedema.

102
Q

what happens due to the fact that a proportion of the stroke volume is regurgitated? and what does this lead to?

A

Since a proportion of the stroke volume is regurgitated, the stroke volume increases to maintain the forward cardiac output and the left ventricle therefore enlarges.

103
Q

what is the increased stroke volume due to regurgitation sensed as?

A

a ‘palpitation’

104
Q

why does dyspnoea and orthopnoea develop with regurgitation?

A

due to pulmonary venous hypertension occurring as a direct result of the mitral regurgitation and secondarily to left ventricular failure

105
Q

what are the signs of mitral regurgitation?

A

- Laterally displaced diffuse apex beat and a systolic thrill.
- Soft first heart sound owing to the incomplete apposition of the valve cusps and their partial closure by the time ventricular systole begins.
- Pan-systolic murmur owing to the occurrence of regurgitation (thus turbulent blood flow) throughout the whole of systole, being loudest at the apex but radiating widely over the precordium and into the axilla.
- Prominent third heart sound, owing to the sudden rush of blood back into the dilated left ventricle in early diastole (sometimes a short mid-diastolic flow murmur may follow the third heart sound). “lubsshhh dub”

106
Q

what’s the link between enlarged left atrium and atrial fibrillation?

A

- The high left atrial pressure in mitral valvular disease also causes progressive enlargement of the left atrium, which increases the distance that the cardiac electrical excitatory impulse must travel in the atrial wall.
- This pathway may eventually become so long that it predisposes to development of excitatory signal circus movements.
- In late stages of mitral valvular disease, atrial fibrillation usually occurs.

107
Q

beta-blockers

  • what used for
  • what do they target
  • what do their targets do and how
  • mechanism of action
  • side effects
A

• These are used to treat the symptoms of heart failure.
• They are also used to treat congestive heart failure and in the management of cardiac arrhythmias, protecting the heart from a second heart attack (myocardial infarction).
• β1 receptors are found in the heart.
• These increase the cardiac output by:
 - Increasing the heart rate in the sinoatrial node (SAN).
 - Increasing the atrial muscle contractility.
 - Increasing the contractility and the automacity of ventricular cardiac muscle.
 - Increasing the conduction and automacity of atrioventricular nodes.
• Mechanism of action:
1. Beta-blockers are β1 receptor antagonists.
2. Reduces heart rate, thus giving the left ventricle more time to fill up.
3. Reduce blood pressure by decreasing the contractility.
 These put less load on the heart.
• Side Effects:
 - Nausea; diarrohea; bronchospasm and dyspnea (if β2 receptor antagonists used); bradycardia; hypotension; heart failure; fatigue; dizziness.

108
Q

carvedilol

  • what is it
  • what used for
  • mechanisms of action
  • side-effects
A

• This is a non-selective beta-blocker (β1 and β2).
• This is also an alpha-1 (α1) receptor blocker.
• It is administered in the treatment of mild to severe congestive heart failure (CHF) and high blood pressure.
• Mechanisms of action:
1. Norepinephrine stimulates the nerves that control the muscles of the heart by binding to the β1- and β2-adrenergic receptors.
2. Carvedilol is an antagonist for these receptors, which both slows the heart rhythm and reduces the force of the heart’s pumping.
3. This lowers blood pressure thus reducing the workload of the heart.

  1. Norepinephrine also binds to the α1-adrenergic receptors on blood vessels, causing them to constrict and raise blood pressure.
  2. Carvedilol is an antagonist for this receptor, which also lowers blood pressure.
    • Side Effects:
     Bronchospasm and dyspnea (β2 receptor);hypotension; diarrohea; bradycardia.
109
Q

Ramipril

  • what is it
  • what used to treat
  • mechanism of action
  • side-effects
A

• This is an ACE inhibitor (Angiotension-Converting Enzyme inhibitor).
• It is used to treat high blood pressure, fluid retention and heart failure.
• Mechanism of action:
1. ACE inhibitors act by interfering with the action of the enzyme that converts the inactive angiotension I to the powerful artery constrictor angiotension II.
2. The absence of ACE allows arteries to widen and the blood pressure to decrease.
• Side effects: dry cough.

110
Q

glyceryl trinitrate

  • what used to treat
  • what is it
  • mechanism of action
  • side-effects
A

• Also known as nitroglycerin.
• It is used mainly to treat heart failure and to prevent and treat angina.
• It is a vasodilator.
• Mechanism of action:
1. It is a prodrug –it must first be denitrated in the liver to produce the active metabolite nitric oxide.
2. The nitric oxide increases the level of cGMP (cyclic guanosine monophosphate) in the smooth muscle cells of blood vessels.
3. This causes activation of intracellular protein kinases in response.
4. These cause relaxation of the vascular smooth muscles, leading to vasodilation and increased blood flow.
• Side Effects:
 Large doses may cause flushing, headache and fainting.

111
Q

Furosemide

  • what used to treat
  • what is it
  • mechanism of
  • side-effects
A

• It is used to treat fluid retention (oedema) associated with congestive heart failure or kidney disease and also sometimes to treat high blood pressure.
• It is a loop diuretic.
• Mechanism of action:
1. Acts on the ascending loop of Henle.
2. Loop diuretics inhibit the sodium-potassium symporter in the ascending loop of Henle.
3. By inhibiting the transporter, these drugs reduce the reabsorption of NaCl.
4. This increases the water potential (and volume of water) in the urinary tract, leading to increased excretion of water (urine).
• Side Effects:
 Nausea; vomiting; hyperglycaemia; hypomagnesemia; hypokalemia.

112
Q

Digoxin

  • what used for
  • what extracted from
  • mechanism of action
  • side-effects
A

• It is used to control atrial fibrillation (AF).
• It is extracted from digitalis (foxglove).
• It is a cardiac glycoside that increases the force of heart contraction and decreases heart rate.
• Mechanism of action:
1. Digoxin binds to the Na+/K+ ATPase pump in the membranes of heart cells (myocytes) and decreases its function.
2. This increases the level of sodium ions in the myocytes.
3. This leads to a rise in the level of intracellular calcium ions.
4. This occurs because the sodium/calcium exchanger on the plasma membrane is dependent on a constant inward sodium gradient to pump out calcium.
5. Increased Ca2+ levels also leads to increased storage of calcium in the sarcoplasmic reticulum, causing a corresponding increase in the release of calcium during each action potential.
6. This leads to increased contractility (the force of contraction) of the heart without increasing heart energy expenditure.
• Side Effects:
 Abnormal heart activity (bradycardia).

113
Q

warfarin

  • what used for
  • what is it
  • mechanism of action
  • how reverse effects of warfarin
  • how is the dosage of warfarin monitored
  • side-effects
A

• It is used mainly in the prevention and treatment or thrombosis and pulmonary embolism.
• It is an anticoagulant.
• Mechanism of action:
1. Warfarin decreases blood coagulation by inhibiting vitamin K1 epoxide reductase.
2. This enzyme recycles oxidised vitamin K1 to its reduced form after it has carboxylated several blood coagulation proteins.
3. The blood coagulation proteins include prothrombin and factors II, VII, IX, X.
4. Warfarin is labelled a vitamin K1 antagonist but it doesn’t antagonise the action of vitamin K1, but rather antagonises vitamin K1 recycling, depleting active vitamin K1.
5. To reverse effects of warfarin, fresh vitamin K1 is given.

• The dosage of warfarin is monitored according to INR measurements:
 - INR: International Normalised Ratio
 - This is the ratio of a patient’s prothrombin time (PT) to standardised ‘normal’ PT.
 - For example, an INR = 2 indicates that the person’s blood takes twice the normal time to clot.
• Side Effects:
 - Haemorrhage.

114
Q

Aldosterone receptor antagonists

  • what used for
  • examples
A

• It is used in the treatment of severe left ventricle dysfunction (EF <35%, NYHA II).
• E.g. eplerenone and spironolactone.
• Mechanism of action:
1. Anti-fibrotic effects (that are caused by aldosterone). (blocks or prevents tissue scarring)
2. Blocks aldosterone receptors, therefore less Na+ and water reabsorption, therefore less fluid retention, therefore reducing venous return and so reducing the workload on the heart.

115
Q

where is the sound of the blood flow (turbulence) heard greatest?

A

in the direction of the blood flow

116
Q

where do you auscultate the heart valves?

A
  • Aortic valve: Right 2nd intercostal space.
  • Pulmonary Valve: Left 2nd intercostal space.
  • Tricuspid Valve: Left 4th intercostal space at the left sternal edge.
  • Bicuspid valve: Left 5th intercostal space at the mid-clavicular line (apex).
117
Q

what is echocardiogram a key role in the investigation of? and what does it provide information relating to? and what do they help define?

A

heart failure

Provides information relating to ‘ejection fraction (EF)’:
 - Normal (approx 60%).

Patients with heart failure subdivided into:
 - HF with preserved LV function (EF >45%)
 - HF with LV systolic dysfunction (EF <45%)

Echocardiography helps define the aetiology of HF:
 Assessment of valves
 Chamber size/ structure etc

118
Q

what should the diameter of a normal heart be?

A

half the diameter of that of the thorax

119
Q

what are indications for recording ECG?

A 
	- Shortness of breath
	- Abnormal rhythm
	- Chest pain
	- Collapse
	- Loss of consciousness
120
Q

what are the rules for the QRS complex?

A

- 1st downward deflection is a Q wave.
- An upward deflection is an R wave, independent of a preceding Q wave.
- Any downward deflection below the base line following an R wave is an S wave.

121
Q

describe an ECG and how it relates to atrial and ventricular pressures

A
  • P wave is caused by spread of depolarization through the atria, and this is followed by atrial contraction, which causes a slight rise in the atrial pressure curve immediately after the electrocardiographic P wave.
  • The QRS waves appear after the P wave as a result of electrical depolarization of the ventricles, which initiates contraction of the ventricles and causes the ventricular pressure to begin rising. Therefore, the QRS complex begins slightly before the onset of ventricular systole.
  • The T wave represents the stage of repolarization of the ventricles when the ventricular muscle fibers begin to relax. Therefore, the T wave occurs slightly before the end of ventricular contraction.
122
Q

what is heart rate in terms of ECG?

A

the number of QRS complexes per minute

123
Q

what are the different chest leads?

A

V1: Right 4th intercostal space.
V2: Left 4th intercostal space.
V3: Between left 4th and 5th intercostal spaces.
V4: Left midclavicular line in the 5th intercostal space.
V5: Left anterior axillary line in the 5th intercostal space.
V6: Left midaxillary line.
(V = vector)

124
Q

what do the different chest leads give information about?

A

 V1 & V2: Right ventricle
 V3 & V4 : Ventricular septum
 V5 & V6 : Anterior & Lateral wall of the Left ventricle

125
Q

what are the different limb leads?

A

- Lead I, lead II and lead III.

- aVR (right arm), aVL (left arm) and aVF (foot).

126
Q

what do the limb leads measure?

A

potential difference between one limb lead and another

127
Q

which areas of the heart do the limb leads give an electrical activity trace of?

A

 aVR : right atrium
 aVL + lead I + lead II : left lateral
 aVF + III: inferior

128
Q

what is sinus rhythm and sinus arrhythmia?

A

 Sinus rhythm: regularly spaced.

 Sinus arrhythmia: irregularly spaced QRS complex

129
Q

what is atrial fibrillation?

  • what are the dangers
  • common causes
A 
- No P wave
- QRS complex of normal shape
- Irregularly irregular pulse
    - Atria not beating in harmony
- Danger of clot formation 
- Common causes: myocardial ischaemia (angina), myocardial infarction
130
Q

what’s ventricular fibrillation?

A

- Fatal
- No recognisable pattern on ECG
- Patient loses consciousness
- Advanced life support needed

131
Q

what happens in the body during heart failure?

A
  1. Reduced cardiac output
  2. Increase sympathetic activity (as body thinks there is blood volume loss)
  3. Reduced renal perfusion
  4. Activation of renin-angiotensin system
  5. Increase angiotensin (peptide hormone that causes vasoconstriction and an increase in blood pressure), increase aldosterone (steroid hormone – main role is to regulate salt and water in body, thus having an effect on blood pressure)
  6. Vasoconstriction – increase afterload
  7. Na and H2O retention
132
Q

what is mitral stenosis?

A

when valves become thickened, scarred and shrink

133
Q

explain the striations of a cardiomyocyte

A
  • Sarcomere: the essential contractile unit of a cardiomyocyte
  • Z-lines are attached to thin filaments (actin)
  • Thin filaments form a ‘sandwich’ with the myosin thick filaments
  • A band is generated by myosin filaments
  • I band is composed mainly of actin filaments
134
Q

describe diastole of the cardiac cycle

A

In phases 5-7:
- Ventricles are relaxed
- Mitral and tricuspid valves open
- Blood flows passively from atria into ventricles
In phase 1:
- Atrial depolarisation -> P wave
- Both atria contract -> ventricles full (LVEDV = 120ml blood)

135
Q

describe systole of the cardiac cycle

A

In phase 2:
- AV valves close
- Ventricles contract, pressure increases, volume unchanged = isovolumetric contraction
- Ventricular depolarisation -> QRS complex
In phase 3-4:
- Outflow valves open
- Blood ejected into aorta and pulmonary artery
- Volume decreases -> LVESV (left ventricle end systolic volume) (50ml)

136
Q

what causes the two heart sounds? when are they produced?

A 
S1 = lub sound = marks the beginning of systole – when the atrioventricular valves close 
S2 = dub sound = marks the end of systole and beginning of diastole – when the semilunar valves close
137
Q

describe how the m and h gates work

A
  • The ion channels, that open and close, use these gradients to move ions across the membrane
  • Have an ion selectivity filter
  • Activation (m) gate – opens when the cell is stimulated, or membrane potential is depolarised (made more positive)
  • Inactivation (h) gate – this starts to close as m gate opens, but only very slowly so that ions can travel through the ion channel once the m gate starts to open and before the h gate closes
  • When h gate closes, you can’t stimulate and open the channel again until the h gate is opened again
  • When the h gate opens, it has recovered from its inactive state (when the h gate is closed the channel is inactive)
  • H gate opens again when the cell’s returned to its resting membrane potential
138
Q

what are inward rectifier K+ channels (Kir) important for?

A

in setting the resting membrane potential

139
Q

what are T-type calcium channels? where are they important?

A
  • Tiny conductance, more negative potentials
  • Important in pacemaker cells
  • Masked by the huge influx in sodium
140
Q

what are the effects of hyperkalaemia on the action potential and excitability?

A

Phase 4
- Resting membrane potential is more positive (depolarised)
- Happened because of loss of K+ gradient
Threshold: all or none
- Patient with hyperkalaemia is closer to the threshold potential
- So cellular excitability is increased
Phase 0
- Rate of rise is proportional to the RMP
- Slightly depolarised RMP affects the ability of h gates to recover from the inactive state, so this means the h gates recover more slowly, so not all the Na channels are ready to fire, so there is an action potential with a slower upstroke – decrease rate of rise of phase 0
Conduction:
Decrease Vmax leads to:
- Slowing of impulse conduction through myocardium -> patients can develop fatal arrhythmias
- Prolongs P wave, PR interval and QRS complex of the ECG
- Can pick up arrhythmias on ECG but not always possible
Hyperkalaemia needs to be treated rapidly and effectively otherwise it can lead to death

Medicine Sem 2 (10 decks)

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