The Heart Flashcards

1
Q
  1. How much of the heart is:
    a) to the right of the midline?
    b) to the left of the midline?
  2. Between which two structures does the right side run?
  3. Between which two structures does the left side run?
  4. In which direction does an increase in heart size occur?
A

1a) 1/3
1b) 2/3
2. 3rd and 6th costal cartilages in the parasternal line
3. between 2nd costal cartilage and 5th intercostal space at the mid clavicular line
4. inferiolateral

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2
Q
  1. What is the function of the fibrous pericardium?
  2. what does the serous pericardium form?
  3. what are the 3 layers of the heart and what is their structure?
  4. name the 2 pericardial sinuses
A
  1. anchors the heart in the mediastinum
  2. double layer of visceral and parietal pericardium
  3. epicardium - visceral pericardium and fibroelastic and adipose tissue
    myocardium - cardiac muscle tissue
    endocardium - endothelium which provides a smooth lining for heart chambers and is continuous with endothelium of great vessels
  4. oblique pericardial sinus
    transverse pericardial sinus
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3
Q
  1. on a chest radiograph, what forms the aortic knuckle?

2. what is the apex of the heart formed by?

A
  1. arch of aorta

2. tip of the left ventricle

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4
Q
  1. what does the right atrium of the heart form?
  2. which vessels drain into the right atrium?
  3. what is the structure of the
    a) posterior wall
    b) anterior wall. Why?
  4. what developmental structure is present in the right atrium?
  5. which valve separates the right atrium and ventricle?
  6. what does the right ventricle form?
  7. what are trabeculae carnae?
  8. what are the cusps of the AV valve connected to? What is the role of this?
  9. What is the septomarginal trabeculae?
  10. What is the infundibulum?
A
  1. right border of heart
  2. coronary sinus and vena cava
    3a) smooth
    3b) rough due to presence of pectinate muscles
  3. fossa ovalis (remnant of foramen ovale)
  4. tricuspid valve
  5. anterior surface of heart
  6. ridges formed by raised bundles of cardiac muscle fibres
  7. chordae tendone > papillary muscles. Prevent the opening of the AV valve under high ventricular pressure
  8. a band that contains the AV bundle
  9. structure from which pulmonary trunk arises
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5
Q
  1. what does the left atrium form?
  2. which vessels drain into the left atrium?
  3. what is the structure of the
    a) posterior wall
    b) anterior wall. Why?
  4. which valve separates the left atrium and ventricle?
  5. what does the left ventricle form?
  6. what 3 anatomical structures does it contain?
A
  1. posterior surface of heart
  2. pulmonary veins
    3a) smooth
    3b) rough due to pectinate muscles
  3. Mitral (bicuspid Valve)
  4. left border and apex of heart
  5. chordae tendonae and papillary muscles
    trabeculae carnae
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6
Q

Where can the following valves be auscultated?

  1. aortic
  2. pulmonary
  3. tricuspid
  4. mitral
A
  1. right sternal border, second intercostal space
  2. left sternal border, second intercostal space
  3. left sternal border, 5th intercostal space
  4. left midclavicular line, 5th intercostal space
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7
Q
  1. What is the anatomical and functional nomenclature for the following coronary sinuses?
    a) right aortic sinus
    b) left aortic sinus
    c) posterior aortic sinus
  2. Which sinuses do the coronary arteries emerge from?
    a) right
    b) left
  3. what is special about the coronary arteries?
  4. Describe the route and branches of the right coronary artery
  5. describe the route and branches of the left coronary artery
  6. Which artery is known as the widow maker and why?
A

1a) anterior aortic sinus
1b) left posterior sinus
1c) right posterior sinus
2a) right aortic/anterior sinus
2b) left aortic/left posterior
3. They are the only arteries to fill during diastole

  1. runs down AV groove. marginal artery branches off along inferior border to Apex
    Supplies SAN and AVN in 60 and 80% of people
  2. bifurcates almost immediately into left anterior descending and left circumflex. Anterior descending passes between RV and LV. Circumflex passes between LA and LV
  3. anterior descending.
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8
Q
  1. Which coronary arteries do these cardiac veins accompany?
    a) great cardiac vein
    b) middle cardiac vein
    c) small cardiac vein
    d) oblique cardiac vein
  2. What do these veins drain into?
A

1a) left anterior descending
1b) posterior descending
1c) marginal artery
d) left atrium
2. coronary sinus

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9
Q
  1. What is the structure of cardiac muscle?
  2. what are cardiac muscle cells called?
  3. what structures connect cardiac muscle cells? What does this enable them to do?
A
  1. striated. Muscle cells are highly branched
  2. cardiomyocytes
  3. intercalated discs - gap junctions and desmosomes. Enables cardiac muscle to act as a syncytium.
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10
Q
  1. What is:
    a) inotropy
    b) lusitropy
    c) chronotropy
    d) dronotropy
  2. What is the effect of the sympathetic nervous system on the heart?
  3. What is the effect of the parasympathetic nervous system on the heart?
  4. What do autonomic neurons synapse onto?
  5. What receptors do adrenaline and noradrenaline act on in the heart? What is the effect of this?
  6. What type of receptors are these receptors? How do they mediate their effects?
  7. What receptors are implicated in parasympathetic control of the heart? What type of receptors are these? How do they mediate their effects?
A

1a) contraction of heart
1b) relaxation of heart
1c) firing rate of SA node
1d) conduction velocity of AV node

  1. positive inotropic, chrontropic and dronotropic effects
  2. negative inotropic, chronotropic and dronotropic effects
  3. SA and AV nodes. Sympathetic efferents also synapse onto cardiomyocytes
  4. Beta1. increase inotropy, chrontropy and dronotropy.
  5. GPCRs. via a cAMP and PKA mediated pathway, induces depolarisation
  6. muscarinic AcH receptors. GPCRs. activate a G protein coupled inward rectifying potassium channel > hyperpolarisation
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11
Q
  1. describe the resting membrane potential of a cardiomyocyte
  2. what mediates the depolarisation phase?
  3. what mediates the notch seen on the cardiac action potential?
  4. what mediates the plateau phase?
  5. what mediates repolarisation?

PACEMAKER CELL AP

  1. Describe the following phases:
    a) phase 4
    b) phase 0
    c) phase 3
A
  1. membrane has low Na and Ca permeability and high K permeability
  2. Na entry via fast voltage gated sodium channels. Membrane potential increases to +60mV
  3. rapid inactivation of fast Nav channels, and brief opening of K+ channels which reduces Vm slightly
  4. opening of slow Cav channels. Sustains action potential. Ca is also required for contraction
  5. opening of Kv channels and closure of SR Ca channels.

6a) slow spontaneous depolarisation until threshold is reached. Reduction of K+ efflux over time and continuous flow of Sodium (funny current)
b) upstroke. Increase in funny current. Opening of Cav channels
c) opening of K leak channels and inactivation of Na and Ca channels. Sodium calcium exchanger pumps Ca out of intracellular space, effectively relaxing cell

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12
Q
  1. Describe the electrical conduction system of the heart
  2. What are the 3 pacemaking tissues?
  3. Why is the SA node the primary pacemaker?
  4. How does AP propagate from SA node to LA and RA
  5. What ensures sequential contraction of the atria and ventricles?
A
  1. SA node > AV node > bundle of His > right and left bundle branches > pukinje fibres
  2. SA node, AV node, bundle of His
  3. it has the fastest frequency of depolarisation
  4. to RA via gap junctions (direct cell to cell pathways)
    to RA via interatrial bachmann’s bundle
  5. the AV node and bundle branches is the only electrical access between atria and ventricles
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13
Q

Describe the stages of the cardiac cycle of the following:

  1. Atrial systole (3)
  2. Ventricular Systole (5)
  3. Diastole (4)
A
    • depolarisation of SA node and subsequent atrial depolarisation
      - atrial depolarisation causes atrial systole
      - contraction of atria exerts pressure on blood, forcing blood through AV valves into ventricles
    • ventricular depolarisation causes ventricular systole
      - contraction of ventricles causes pressure to rise. Blood pushes up against AV valves forcing them shut
      - Isovolumetric contraction
      - sharp pressure increase causes ventricular pressure to exceed that of arteries - semilunar valves open and blood is ejected
    • ventricular repolarisation causes ventricular diastole
      - fall in ventricular pressure. Blood in arteries begins to fall back. This backflow closes SL valves - dicrotic notch
      - isovolumetric relaxation
      - atrial pressure exceeds ventricular pressure - AV valves open and ventricular filling occurs
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14
Q
  1. What is cardiac output?
  2. What is stroke volume?
  3. what is stroke volume determined by?
  4. what is the ejection fraction?
  5. Name 3 factors that influence stroke volume
  6. Name 2 factors that influence heart rate
A
  1. stroke volume x heart rate
  2. the volume ejected by each ventricle during each contraction
  3. end diastolic volume - end systolic volume
  4. the fraction of the end diastolic volume that is ejected out by each ventricle per beat
  5. preload - stretch. Frank Starling. Proportional to end diastolic volume (which is determined by venous return and duration of diastole)
    contractility
    Afterload - pressure that must be overcome for SL valves to open
  6. autonomic innervation
    hormones - adrenaline, thyroid hormones and catecholamines increase; oxytocin decreases
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15
Q
  1. what produces the:
    a) P wave
    b) QRS complex
    c) T wave
  2. what is the:
    a) ST segment?
    b) QT interval
A

1a. Atrial depolarisation
1b. ventricular depolarisation
Q - interventricular septum
R - apex and free walls
S - base regions
1c) Ventricular repolarisation

2a) period between end of ventricular depolarisation and beginning of ventricular repolarisation
2b) time taken for ventricles to depolarise and then repolarise.

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16
Q
  1. On an ECG, what is the duration of 1 big square; 5 big squares?
  2. How can HR be determined from an ECG?
A
  1. 1 big square = 0.2 secs; 5 big squares = 1 sec

2. counding the number of big squares between an RR interval

17
Q
  1. What is atrial fibrilation characterised by?
  2. Name symptoms of an atrial fibrilation episode
  3. How does atrial fibrilation occur?
  4. What are the ECG characteristics of atrial fibrilation?
  5. Name causes of atrial fibrilation
  6. Name 4 treatments of atrial fibrilation
A
  1. rapid and irregular beating of the atria
  2. heart palpitations, fainting, lightheadedness, SOB and chest pain
  3. normal regular SA impulses are overwhelmed by disorganised electrical impulses originating in the roots of pulmonary veins. Leads to irregular conduction of ventricular impulses that generate heartbeat.
  4. no P waves. F waves present. irregularly irregular R waves
  5. idioppathic. ischaemic heart disease. Hypertension. Valvular heart disease. Alcohol. Thyrotoxosis. Cardiomopathy
  6. beta blockers. digoxin. anticoagulants. cardioversion.
18
Q

How does digoxin work?

A

inhibits Na/K ATPase. Sodium can’t be extruded so intracellular sodium increases. Inhibits the function of NCX, which pumps Ca out of the cell in exchange for Na. Calcium is not extruded, leads to increased Ca uptake into SR. Increased SR stores allow for greater Ca release upon depolarisation - faster and more powerful contraction is achieved and refractory period of AV node is increased.

19
Q
  1. What is the JVP?
  2. What does the JVP tell us?
  3. What can a raised JVP indicate?
  4. JVP waveform:
    a) a
    b) x descent
    c) C
    d) v
    e) y
A
  1. pulse in the internal jugular.
  2. tells us about pressure in RA
  3. fluid overload which increases pressure in the right atrium

4a) peak in pressure caused by atrial systole
4b) atrial diastole
4c) closure of tricuspid valve which bows into RA. Causes a slight decrease in volume thus increase in pressure
4d) pressure increases with venous return against closed tricuspid valve
4e) opening of tricuspid valve

20
Q
  1. What are the following heart sounds caused by?
    a) S1
    b) S2
    c) S3
    d) S4
  2. What is S2 splitting?
  3. What are the following defects and what murmurs do they cause?
    a) aortic stenosis
    b) aortic regurgitation
    c) mitral stenosis
    d) mitral regurgitation
A

1a) closure of AV valves
1b) closure of SL valves
1c) ventricular filling in early diastole
1d) ventricular filling as atria contract

  1. splitting of S2 sounds as chest wall expands and causes intrathoracic pressure to become more negative. This induces an increase in venous return to the right side and a decrease in return to the left side.
    Pulmonary valve stays open longer during ventricular systole.

3a) turbulant blood flow through stiffened aortic valve. Mid systolic murmur
3b) turbulent blood flow through leaky aortic valve. early diastolic murmur. Lower pitch
3c) turbulant blood flow through stiffened mitral valve. mid to late systolic murmur
3d) turbulent blood flow through leaky mitral valve. Heard immediately after S1.