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HYMS Y1 > Block 2 W3 > Flashcards

Block 2 W3 Flashcards

1
Q

Describe the surface anatomy of the heart.

A

Runs inferolaterally to left.
Right side - between 3rd and 6th costal cartilage parasternal line.
Left side - between 2nd CC and 5th intercostal space midclavicular line.
1/3 is right and 2/3 is left of midline.
Posterior surface - T5 to T8.

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2
Q

Describe the pericardium.

A

Fibroserous sac that encloses the heart and the roots of great vessels (middle mediastinum).
Made up of fibrous pericardium and serous (parietal + visceral) pericardium.

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3
Q

Outline the layers of the pericardium.

A

Fibrous pericardium -> parietal pericardium -> pericardial cavity -> visceral pericardium (epicardium) -> myocardium -> endocardium.

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4
Q

Define pericardial cavity.

A

Potential space between the parietal and visceral layers of pericardium.
Contains serous fluid to prevent friction.

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5
Q

Define fibrous pericardium.

A

Tough, inelastic, dense irregular connective tissue.

Prevents overstitching, protection and anchors to mediastinum.

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6
Q

Define parietal pericardium.

A

Lines the walls of pericardium cavity. Fused to fibrous pericardium.

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7
Q

Define visceral pericardium.

A

Lines the heart and roots of great vessels.

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8
Q

Define the myocardium.

A

Composed of cardiac muscle cells, 95% of heart wall.

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9
Q

Define endocardium.

A

Provides smooth lining for chambers of the heart.

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10
Q

Define the transverse pericardial sinus.

A

Posterior to ascending aorta and pulmonary trunk, anterior to SVC and superior to left atrium.
Separates the arteries and veins.

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11
Q

Define the oblique pericardial sinus.

A

Posterior to heart, between 2 pulmonary veins.

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12
Q

List the cardiac surfaces.

A
  • anterior (sternocostal) -> right ventricle
  • posterior (base) -> left atrium
  • inferior (diaphragmatic) -> left and right ventricles
  • right pulmonary - right atrium
  • left pulmonary - left ventricle
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13
Q

List the cardiac borders.

A

Right border - right atrium
Inferior border - left and right ventricle
Left border - left ventricle
Superior border - left and right atrium and great vessels.

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14
Q

Define aortic knuckle.

A

Contour of the aortic arch seen in an anteroom-posterior radiograph.

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15
Q

What are the chambers of the heart?

A 
Atria:
- thin walls
- receiving chambers functioning to fill ventricles
- vital in setting cardiac pace (60bpm)
Ventricles:
- thick muscular walls
- main pumping (discharging chambers)
- slow beat (40bpm)
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16
Q

Describe the contents of the right atrium.

A

Larger and thinner walls.
- SVC, IVC and coronary sinus drain into this.
- right auricle
- sinus venarum - posteriorly situated smooth wall (receives all vessels)
- musculi pectinati - creates the rough wall
- crista terminalis - separates the rough and smooth walls, provides origin of pectinate muscles.
- sulca terminalis - indicates crista terminalis on exterior.
- fossa ovalis - depression on interatrial septum, represents site of foramen ovale from embryo.
Empties into RV via tricuspid valve

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17
Q

Describe the contents of the left atrium.

A

Smaller and thicker walls
4 pulmonary veins drain here from lungs.
Smooth walls.
Empties into LV via mitral valve (bicuspid).

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18
Q

Describe the contents of the right ventricle.

A

Thinner walls
- trabeculae carneae cordis - anastomosing prominent muscular ridges of myocardium, prevents heart wall sticking together when contracting.
- papillary muscles - cone-shaped muscles extending from ventricular wall to chordae tendineae, contracts to prevent valve opening and regurgitation of blood.
- chordae tendineae - extends from papillary muscle to cusps of valve.
- conus arteriosus (infundibulum) - upper smooth-walled portion leading to pulmonary trunk.
- septomarginal trabecula (moderator band) - between IV septum and anterior papillary muscle.
- IV septum
Empties into pulmonary artery via pulmonary valve.

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19
Q

Describe the contents of the left ventricle.

A

Thicker walls
Divided into ventricle proper and aortic vestibule.
Has 2 papillary muscles with their chordae tendineae and meshwork of trabeculae carneae chordis.
Empties into aorta via aortic valve.

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20
Q

What are the atrioventricular valves?

A

Tricuspid and mitral valves.

Requires papillary muscles and chordae tendineae to open and close.

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21
Q

What are the semilunar valves?

A

Pulmonary and aortic valves.
No chordae tendineae or papillary muscles.
Tricuspid.

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22
Q

Where are the valves most audible?

A

Tricuspid - lower end of sternum
Mitral - left 5th intercostal space, midclavicular line
Pulmonary - left 2nd intercostal space
Aortic - right 2nd intercostal space

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23
Q

Describe the coronary arteries.

A

Blood supply to heart muscles.
Right and left coronary arteries come off ascending aorta.
Only arteries to fill during diastole.
Position of coronary arteries and opening of the aortic valve prevents blood flow into coronary circulation during systole.

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24
Q

Describe the right coronary artery.

A

Originates from right aortic sinus.
- runs down atrioventricular groove
- supplies right atrium, right ventricle and posterior 1/3 IV septum
- supplies sinoatrial nodal artery (60%) and atrioventricular nodal artery (80%)
Gives rise to:
- marginal artery - inferior right border (L-shape) right ventricle
- posterior descending artery (85%) left ventricle

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25
Q

Describe the left coronary artery.

A

Originates from left aortic sinus.
- large but shorter as bifurcates
- supplies left atrium, left ventricle and anterior 2/3 IV septum
Gives rise to:
- left anterior descending artery (anterior IV)
- left circumflex artery

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26
Q

Why is the anterior descending artery termed the “widow maker”?

A

Major site for occlusion -> heart attack.

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27
Q

Describe the venous drainage of the heart.

A

Cardiac veins accompany coronary arteries:
- great CV -> left anterior descending
- middle CV -> posterior descending
- small CV -> marginal
- oblique CV -> descends from left atrium
Great + middle + small + oblique drain into coronary sinus -> right atrium.
- anterior CV - collects blood from right ventricle and drains into right atrium.
- smallest (thebesian) CV - return blood directly to heart chambers.

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28
Q

Describe the position of the coronary sinus.

A

Lies in coronary sulcus - separates atria from ventricles.

Opens into right atrium.

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29
Q

Describe the lymphatic drainage of the heart.

A

Right CA -> anterior mediastinal nodes

Left CA -> trachea bronchial node.

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30
Q

Describe the innervations of the heart.

A

Superior cardiac plexus

Deep cardiac plexus

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31
Q

Describe the cardiac muscle.

A

Striated, branching, numerous mitochondria and less nucleated than skeletal muscles.
Cardiac muscle cells are interconnected together by intercalated discs.

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32
Q

What do intercalated discs contain?

A

Gap junction -> functional syncytium, allows APs to propagate faster and enables cardiac muscles to contract together.
Desmosomes -> attach adjacent cardiac muscle cell together.

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33
Q

Describe the consequences of sympathetic activation on the heart.

A

Positive inotropic effect.
Sympathetic activation -> releases NA and adrenaline ->
- Ca2+ channels open and trigger influx of Ca2+ and induces Ca2+ release from SR -> binds troponin C -> cross-bridge cycling.

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34
Q

What does lusitropy (relaxation) require?

A

2 transporters to remove Ca2+ from sarcoplasm:

  • sarcoendoplasmic reticulum calcium ATPase (SERCA) returns Ca2+ to SR.
  • Na+/Ca2+ exchanger in sarcolemma transports Ca2+ out of cell.
35
Q

Explain the cardio-inhibitory and excitatory centres of the brain.

A

Medulla - autonomic control of heart:

  • cardio-inhibitory centre (parasympathetic) -> vagus nerve -> innervates SAN and AVN -> reduces heart contraction.
  • cardio-excitatory centre (sympathetic) -> thoracic spinal cord -> sympathetic chain ganglion -> sympathetic cardiac nerve -> innervates SAN and AVN -> increases heart contraction.
36
Q

Describe the mechanism of action of NA on SA node cells.

A

NA binds to beta1 receptors, coupled to Gs on G protein -> adenylate cyclase converts ATP -> cAMP (2nd messenger) -> activates protein kinase.
Causes funny channel and T-type Ca2+ channels to open -> Na+ and Ca2+ influx -> depolarisation.
Positive chronotropic, inotropic, dromotropic and lusitropic effects.

37
Q

List the roles of active protein kinase.

A
  • L-type Ca2+ channels open on sarcolemma
  • calcium induced calcium release from SR
  • enhanced actin-myosin interaction
  • Ca2+ pumped back into SR
38
Q

Describe the mechanism of action of ACh on SA node cells.

A

ACh binds muscarinic M2 cholinergic receptor, coupled to Gi on G protein.
Inhibits T-type Ca2+ channel (no influx) and activates K+ channels (GIRK) for K+ efflux -> hyperpolarisation.
Negative chronotropic, inotropic, dromotropic and lusitropic effects.

39
Q

Describe the sinoatrial node.

A

Pacemaker of heart.

Exhibits phase 4 depolarisation or automaticity. AV node and His-Purkinje system are latent pacemakers.

40
Q

Outline the action potential of the SAN.

A

Phase 4 ->
- slow depolarisation
- increase in Na+ conductance -> pacemaker Na+ influx
- Ca2+ channels recover from inactivation
- pumps restore ion gradients
Phase 0 ->
- Ca2+ influx -> depolarisation.
Phase 3 ->
- Ca2+ channels inactivate
- delayed K+ efflux -> gradual depolarisation.

41
Q

Describe the action potential of the ventricular cells.

A 
Phase 4 ->
- resting membrane potential
- Na+ and Ca2+ channels recover from inactivation
- pumps restore ion gradients
Phase 0 ->
- Na+ influx -> depolarisation
Phase 1 ->
- initial repolarisation
- Na+ channels inactivate
- fast K+ efflux
Phase 2 -> 
- Ca2+ influx -> depolarises again
Phase 3 -> 
- Ca2+ channels inativate
- delayed K+ efflux -> repolarisation.
42
Q

Explain the conduction pathway.

A

SAN -> AVN -> bundle of His -> left and right bundles -> Purkinje fibres.

43
Q

What are the durations of the cardiac cycle?

A

Atrial systole -> 0.1s
Ventricular systole -> 0.3s
Diastole -> 0.4s
0.8s

44
Q

Describe the cardiac cycle.

A
  1. atrial systole
    a. end-diastolic volume 135ml.
  2. isovolumic ventricle contraction
  3. ventricular ejection
    a. end-systolic volume 65ml
  4. isovolumic ventricle relaxation.
  5. rapid ventricular filling
  6. late diastole
45
Q

What happens in atrial systole?

A

After P wave (atrial depolarisation)

Atrial contraction forces small amount of blood into ventricle -> increase in atrial pressure (a wave).

46
Q

What happens in isovolumic ventricular contraction.

A

QRS complex (ventricular depolarisation)
When ventricular pressure becomes greater than atrial pressure, mitral valve close -> 1st heart sound.
Ventricular pressure increases isovolumetrically as result of ventricular contraction but no blood leaves ventricles as aortic valve is closed.

47
Q

What happens in ventricular ejection?

A

Ventricular pressure reaches max. C wave - bulging of tricuspid valve into right atrium.
When ventricular pressure becomes greater than aortic pressure -> aortic valve opens.
Rapid ejection of blood into aorta due to pressure gradient.
Ventricular volume decreases rapidly.
Atrial filling begins
T wave - ventricular repolarisation.

48
Q

What happens in isovolumic ventricle relaxation?

A

Aortic valve closes -> 2nd heart sound.
Mitral valve remain closed -> ventricular volume constant as all valves closed.
Ventricular pressure decreases rapidly as ventricles are relaxed.

49
Q

What happens in rapid ventricular filling?

A

When ventricular pressure becomes less than atrial pressure -> mitral valve opens.
Ventricular filling from atrium commences.
Aortic pressure continues to decrease as blood runs off to smaller arteries.
Rapid blow from atria to ventricle causes 3rd heart sound -> pathological in adults not children.

50
Q

What happens in late diastole?

A

Longest phase.

Ventricular filling continues at slower rate.

51
Q

Describe the jugular venous pressure graph.

A

A - atrial contraction, pressure increases.
X - atrial relaxation, descent.
C - ventricular contraction, bulging of tricuspid valve so pressure increases slightly.
X - further ventricular contraction, downward movement of tricuspid valve, descent.
V - passive atrial filling.
Y - atrial emptying with opening of tricuspid valve.

52
Q

Define cardiac output.

A

Product of heart rate and stroke volume.
CO = HR x SV
At rest - 5L/min
Exercise - increases 5-6 fold.

53
Q

Define stroke volume.

A

Volume ejected by each ventricle during each contraction.
SV = EDV - ESV
SV = 120 - 50
SV = 70ml

54
Q

Define ejection fraction.

A

Fraction of EDV ejected out by each ventricle per beat.
EF = SV/EDV

Normal is 55-75%.
Reduced seen in heart failure.
Measures ventricular performance.

55
Q

Describe the Frank-Starling relationship.

A

As EDV increases -> SV increases.
Increases in EDV cause an increase in ventricular fibre length, which produces an increase in developed tension.
Matches CO to EDV.
Changes in contractility shifts the curve upwards (increased contractility) and downward (decreased contractility).

56
Q

Define preload.

A

End-diastolic volume.

57
Q

Define after load.

A

Aortic pressure - resistance ventricle must overcome to circulate blood.

58
Q

How does preload affect SV?

A

Increased preload -> increased SV due to increased EDV.

59
Q

How does after load affect SV?

A

Increased after load -> reduced SV due to ventricle must eject blood against high aortic pressure -> increased ESV.

60
Q

How does contractility affect SV?

A

Increased contraction -> increased SV as ventricle develops greater tension than usual -> decreased ESV.

61
Q

What are the different types of cardiac cells?

A

Myocardial cells - generate pumping pressure, cells connected by intercalated discs with gap junctions.
Conduction cells - rapidly spreading electrical signals to myocardial cells to coordinate pumping.
- pacemaker cells -> SA node and AV node.
Conduction pathway cells - bundle of His and Purkinje fibres.

62
Q

How do pacemaker cells generate auto-rhythmicity?

A

Pacemaker cells generate APs spontaneously due to unstable membrane potential.
Depolarise slowly, reach threshold and trigger AP then return to initial membrane potential -> start again.

63
Q

What determines the sinus rhythm?

A

Pacemaker potential determines rate of firing of SAN - auto-rhythmicity generates normal heart rhythm -> sinus rhythm.

64
Q

What is the rate of auto-rhythmicity of the different cardiac cells?

A

SAN - 110-120 bpm
AVN - 50 bpm
Purkinje fibres - 30-40 bpm

65
Q

What is the conduction velocity of the different cardiac cells?

A

SAN to atrial muscle and AVN = very fast
Bundle of His and left & right bundle branches = slower
Ventricular muscle = faster
Purkinje fibre = slowest

66
Q

Describe the effect of PNS and SNS on conduction.

A

PNS - hyperpolarisation longer and at more negative membrane potential -> slower depolarisation.
SNS - reduced hyperpolarisation -> at less negative membrane potential -> faster depolarisation.

67
Q

What is the effects of NE on B1-adrenoceptors?

A

Adrenaline acts on B1-adrenoceptors via cAMP:
- increases rate of SAN (+ chronotropic)
- increases force of contraction of atrial muscles (+ inotropic)
- increases automaticity of AVN
- increases automaticity and force of ventricular muscle (+ inotropic)
B1-adrenoceptors blocked by B-blockers e.g. propranolol.

68
Q

Define electrocardiogram, ECG.

A

Recording of the electrical activity of heart. Net sum of depolarisation and repolarisation potentials of all myocardial cells.

69
Q

Describe the ECG.

A

P wave - atrial depolarisation (atrial depolarisation buried in QRS complex).
PR interval - depolarisation from SA -> AV
QRS complex - ventricular depolarisation
QT interval - entire period of depolarisation and repolarisation of ventricles
ST interval - period between end of ventricular depolarisation and beginning of ventricular depolarisation
T wave - ventricular repolarisation
U wave - papillary repolarisation

70
Q

Describe the membrane potential at each phase of cardiac muscle AP.

A

Rest - muscle polarised, inside negative and outside positive -> isoelectric.
Depolarising - membrane potential negative -> positive.
Depolarised - inside positive and outside negative.
Repolarising - membrane potential positive -> negative.
Repolarised - inside negative and outside positive -> isoelectric.

71
Q

Describe the direction of cardiac muscle depolarisation.

A
  1. depolarise atria
  2. depolarise septum from left to right
  3. depolarise antero-septal region of myocardium toward apex
  4. depolarise bulk of ventricular myocardium, from endocardium -> pericardium
  5. depolarise posterior portion of base of left ventricle
  6. ventricles all depolarised.
72
Q

What are the 12 ECG leads?

A

Limb leads:
Bipolar leads - limb leads -> leads 1, 2 and 3
Unipolar leads - augmented leads, aVR, aVL and aVF
Chest leads:
V1-V6

73
Q

How is the cardiac rhythm identified from an ECG?

A

Identified from whichever lead shows the P wave more clearly - usually lead 2.

74
Q

Describe the cardiac axis.

A

The cardiac axis is a hexaxial reference system.
Normal cardiac axis lies -30 - 100 degrees.
0 reference point - looks at heart from same viewpoint as lead 1.
Left lower - normal axis
Left upper - left axis deviation
Right lower - right axis deviation
Right upper - extreme.
Axis deviation - useful in diagnosis.

75
Q

How to interpret ECG?

A

Examine trace for: rate, rhythm, cardiac axis, waveform + intervals.
1 square - 0.2s and 0.5mV
2 vertical square - 0.2s and 1mV
5 squares - 1s and 0.5mV

76
Q

Define sinus rhythm.

A

All complexes normal and evenly spaced.

Rate - 60-100beats/min

77
Q

Define atrial fibrillation and describe the ECG findings.

A

Multiple foci in atria fire continuously in a chaotic pattern, causing a totally irregular, rapid ventricular rate.
Pathway conduction problem - re-entry circuits.
Chaotic signals passing though AV node -> rapid ventricular impulses.
ECG:
- QRS complex - irregular
- no P wave
- irregularly irregular

78
Q

What are the causes of AF?

A

Idiopathic, heart disease, pericarditis, pericardial trauma, pulmonary disease, hyperthyroidism/hypothyroidism, systemic illness, stress, alcohol, sick sinus syndrome, pheochromocytoma.

79
Q

What are the types of AF?

A
  1. Paroxysmal - lasts <48 hours
  2. Persistant - >7 days, required cardioversion
  3. Long-standing persistent - must restore sinus rhythm
  4. Permanent - no cardioversion.
80
Q

What are the treatment options for AF?

A

Control ventricular rate and prevent thrombo-emolism.

  1. Beta-blockers
  2. Non-dihydropyridine Ca2+ channel antagonists (verapamil)
  3. Digoxin - reduces number of atrial impulses propagated to ventricles -> use if elderly/sedentary.
  4. Anticoagulants - warfarin or novel oral anticoagulant (NOAC - apixaban)
  5. Rhythm control - cardioversion or amiodarone.
81
Q

What is the mechanism of action of digoxin?

A

Inhibits Na+/K+ ATPase but increases Na+/Ca2+ exchanger -> more Ca2+ influx -> increased TnC Ca2+ binding -> increased inotropy.
- Negative chronotropy -> reduces SAN firing rate
- Negative dromotropy -> reduces conduction velocity of electrical impulses through AVN.
Reduces ventricular rate.

82
Q

What are atrial extrasystoles and what is the ECG findings.

A

Ectopic early beat arises within atria, firing on its own.
ECG:
- early P wave
As this originates within atria not sinus node.
No significance - normal heart but may be precursor to ischaemia.

83
Q

What are ventricular extrasystoles and what is the ECG findings?

A

Ectopic early beat fires on its own from a ventricular focus then spreads throughout ventricle.
ECG:
- wide QRS >0.12s
- no P wave
- inverted T wave
Normal but must be monitored for frequency.

HYMS Y1 (25 decks)

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