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BS > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Stenosis…

A

Leads to decreased blood flow, and establishes a collateral circulation

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2
Q

What does the lymphatic system transport?

A

Interstitial fluid
Bacteria
Cellular debris
Cells eg lymphocytes

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3
Q

Functions of the cardiovascular system (x 6)

A 
Distribute metabolic substrates to the tissues
Removal of waste
Movement of immune cells
Regulation of body water
Maintain internal temperature
Transport signalling molecules
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4
Q

What are the 3 types of pacemaker?

A

Main= sino-atrial node
Secondary- atrio-ventricular node
Back-up= myocytes

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5
Q

Electrical impulse

A
  1. AP initiated in SA node -> AV node
  2. Cells of AV slow the impulse
  3. -> ventricles via bundle of His
  4. AV bundle divides into L and R branches
  5. Spread to contractile cells of ventricle via Purkinje fibres
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6
Q

What is the function of gap junctions?

A

Allow spread of AP through myocardium

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7
Q

What is the refractory period?

A

Gap between heart beats to prevent tetanic contraction

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8
Q

Sinus arrythmia

A

Slowing of SA node on expiration, speeds up on inspiration

Helps preserve cardiac output

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9
Q

Complete heart block

A

Top and bottom of heart are not electrically connected => independent QRS

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10
Q

Ectopic beat

A

Extra heart beat => wider QRS

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11
Q

Atrial fibrilation

A

Strain on the top of heart => irregularly irregular beat

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12
Q

Ventricular fibrilation

A

Completely disorganised contraction => no QRS

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13
Q

Cardiac cycle

A
  1. Diastolic ventricular filling
  2. Isovolumic contraction
  3. Systolic ejection
  4. Isovolumic relaxation
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14
Q

Diastolic ventricular filling

A

Aortic valves open

Atria contract to fill

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15
Q

Isovolumic contraction

A

Aortic valves shut

Pressure but no flow

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16
Q

Systolic ejection

A

Valves open

Blood pushed out

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17
Q

Isovolumic relaxation

A

Early diastole

Valves shut

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18
Q

Cardiac power

A

= force x velocity

= pressure x flow rate

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19
Q

Stroke volume (SV)

A

= End diastolic volume (EDV) x end systolic volume (ESV)

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20
Q

Ejection fraction (LVEF)

A

= SV / EDV

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21
Q

Cardiac output (CO)

A

= heart rate x stroke volume

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22
Q

Blood pressure

A

Force exerted per unit blood

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23
Q

Variables for haemodynamics (x 7)

A 
Heart rate
Blood pressure
Volume
Flow
Blood velocity
Power
Vascular resistance
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24
Q

What does the endoderm induce in vasculogenesis?

A

Mesoderm (visceral/splanchnic) -> angioblasts -> endocardial tubes

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25
Q

What do the endocardial tubes fuse laterally to form?

A

Primitive heart tube

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26
Q

What does the endocardium become?

A

Endothelial lining of the heart

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27
Q

What does the myocardium become?

A

The muscular wall of the heart

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28
Q

What does the epicardium become?

A

The outer surface of the heart and the coronary arteries

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29
Q

What is the function of cardiac jelly?

A

To separate the myocardium and endocardium

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30
Q

Which vessels are at the cranial end of the developing heart?

A

2 dorsal aortae -> 1 aorta

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31
Q

Which vessels are at the caudal end of the developing heart?

A

Sinus venosus (common cardinal, umbilical and vitelline veins)

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32
Q

Which 5 dilations does the heart tube grow into?

A 
Ventricle
Atrium
Sinus venosus
Truncus arteriosus
Conus arteriosus
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33
Q

When does the heart tube fold into 4 chambers?

A

Day 23

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34
Q

Where does the bulbus cordis move?

A

Caudally, ventrally and to the R

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35
Q

Where does the primitive ventricle move?

A

To the L

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36
Q

Where does the primitive atrium move?

A

Cranially and dorsally

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37
Q

What forms the smooth walls of the ventricle?

A

Conus arteriosus

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38
Q

What forms the trabeculated part of the ventricle?

A

Primitive ventricle

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39
Q

How do the atria form?

A

LA wall outgrows into 1 pulmonary vein -> L and R -> bifurcate into 4

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40
Q

What happens to the left atrium at week 5?

A

Veins are intusscepted into the LA wall

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41
Q

When does septation occur?

A

Week 4

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42
Q

Interatrial septation

A

Septum primum divides atria and extends => foramen primum.

AV boundary lining -> dorsal/ventral cushions -> AV septum

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43
Q

At what week do the septum primum and AV septum fuse?

A

Week 6

44
Q

By what week does the sinus venosus degenerate?

A

Week 5

  • R horn -> smooth part of RA wall
  • L horn -> oblique vein of RA and coronary sinus
45
Q

How does the foramen secundum form?

A

From the apoptosis of the septum primum

46
Q

How does the septum secundum form?

A

From the dorsal wall of the atrium

- opening in it forms the foramen ovale

47
Q

Interventriuclar septation

A

Muscular projection from the floor -> endocardial cushions. Leaves interventricular foramen- membranous part projects to close

48
Q

Contruncal septation

A

Truncus arteriosus divided into 2 by conotruncal swellings -> fuse to form sprial septum (separates pulm. trunk and aorta)

49
Q

In the foetus, how does blood pass from RA to LA?

A

Via the foramen ovale

50
Q

Where does the poorly oxygenated blood in the RA pass through?

A

Ductus arteriosus

51
Q

Ductus venosus ->

A

Ligamentum venosum

52
Q

Foramen ovale ->

A

Fossa ovalis (greater pressue in LA on 1st breath)

53
Q

Ductus arteriosus ->

A

Ligamentum arteriosum (increase in O2 sats, decrease in prostaglandins)

54
Q

Dextrocardia

A

Abnormal cardiac looping or induced in gastrulation (wk 5). - associated with abnormal bv connection or septation

55
Q

Patent ductus arteriosus

A

Allows blood to shunt aorta -> pulm artery => increase workload of heart => hypertension, ventricular hypertrophy and heart failure

56
Q

Treatment of patent ductus arteriosus

A

Prostaglandins

57
Q

Atrial septal defects

A

Failure of septa 1 and 2 to close at birth, due to probe patent foramen ovale

58
Q

When is surgery required for atrial septal defects?

A

When pulmonary hypertension occurs

59
Q

Ventricular septal defects

A

Allows L to R shunt of blood => RV hypertrophy and pulmonary hypertension

60
Q

Which ventricular septal defect will resolve as the child grows?

A

Muscular

61
Q

What are conotruncal defects due to?

A

Abnormal migration of neural crest cells

62
Q

Persistent truncus arteriosus

A

Conotruncal septum is absent -> cannot fuse with IV septum

Blood mixes -> poor O2 delivery => cyanosis, breathlessness, lethargy and delayed growth

63
Q

Transposition of the great vessels

A

Conotruncal septum is straight, so aorta from RV and pulm artery from LV
Incompatible with life unless accompanying shunt

64
Q

Tetralogy of Fallot

A

Unequal division of truncus arteriosus

65
Q

What are the 4 features of tetralogy of Fallot?

A

Pulmonary stenosis
VSD
Overriding aorta
RV hypertrophy

66
Q

What is coarctation of the aorta?

A

Narrowing near the ductus arteriosus

67
Q

Preductal coarctation

A

DA obliterates -> hypoperfusion of lower body

Prostaglandins needed to keep DA open

68
Q

Postductal coarctation

A

Collateral circulation established

69
Q

What enters cardiac muscle to initiate contraction?

A

Calcium

70
Q

Cardiac functional reserve

A

The capacity to augment performance on demand eg exercise, illness and pregnancy

71
Q

Cardiac reserve

A

Max cardiac output - cardiac output at rest

72
Q

What is the effect of autonomic input on stroke volume?

A

Prolonged opening of Ca channels -> enhanced action of contraction coupling mechanisms

73
Q

What do small changes in sarcomere length lead to?

A

Large variations in tension

74
Q

What is the effect of stretching the LV?

A

Aids contraction -> increase in preload -> increased performance

75
Q

How does muscle stretching lead to more contraction?

A

The myofibril is reduced -> filaments are closer together -> more myosin/actin interaction => more contraction

76
Q

What causes a L shift on the Frank-Starling curve?

A

Exercise, adrenalin/noradrenaline pharma stimulation

77
Q

What causes a R shift on the Frank-Starling curve?

A

Myocardial loss and pharma depression

78
Q

When is preload best measured?

A

At end diastolic volume

79
Q

How to NAd/Ad cause L shift?

A

Stimulate cAMP -> more calcium entry -> more cross linking

80
Q

How does the body compensate for a failing ventricle?

A

The SNS overactivates, and RAAS systems kicks in to increase preload -> LV stretch

81
Q

Mean systemic arterial pressure=

A

CO x total peripheral resistance

82
Q

How is preload increased? (x 6)

A 
Increased circulating vol
Decreased venous compliance
Increased atrial filling and contraction
Decreased heart rate
Increased ventricular compliance
Increased aortic/pulmonary pressure
83
Q

What is the Bowditch effect?

A

Increase in HR -> increased force of contraction

84
Q

Systemic sympathetic actions

A

RAAS activation -> increased central venous P and total peripheral resistance
Suprarenal stimulation -> catecholamines

85
Q

What are the effects of angiotensin II?

A

Vasoconstriction

Salt and water retention

86
Q

What are the effects of aldosterone?

A

Salt and water retention

87
Q

What is the effect of vasopressin (ADH)?

A

Water retention

88
Q

What are the parasympathetic actions on the heart?

A

Lower heart rate (chronotrophy)
Decreased AV conduction (dromotrophy
Decreased atrial contractility (inotrophy)

89
Q

What are the sympathetic actions on the heart

A

Increased heart rate (chronotrophy)
Increased AV conduction (dromotrophy)
Increased atrial contractility (inotrophy)
Increased myocardial relaxation (lusitrophy)

90
Q

Receptors in the heart

A

B1/2- stimulate NAd release
A2- inhibit NAd release
B1- stimulates contraction

91
Q

Receptors in blood vessels

A

B1/2 and A2- stimulate NAd release
A1- stimulates contraction
B1- stimulates relaxation

92
Q

A1 adrenergic receptors

A

For hypertension- inhibit peripheral motor tone

93
Q

Non-selective B2 antagonists

A

Hypertension and angina (lower heart rate and contractility)

94
Q

Non-selective B1/A1 antagonists

A

Heart failure and severe hypertension

95
Q

B1 selective antagonists

A

Hypertension and angina

eg. atenolol

96
Q

Side effects of beta blockers

A

Bronchoconstriction, heart failure, bradycardia, hyperglycaemia, fatigue and cold extremities

97
Q

Calcium channel blockers

A

Act on smooth and cardiac muscle to reduce vascular tone and contractility
eg. amlodipine and veramapril

98
Q

ACE inhibitors

A

Stop conversion of angiotension I -> II. For hypertension, LV hypertrophy and to prevent a secondary MI
eg. ramipril, lisinopril

99
Q

Angiotensin II receptor blockers

A

Prevent vasoconstriction, reduced ADH and aldosterone secretion. For hypertension, heart failure and nephropathy
eg. valsartan, losartan

100
Q

Nitrovasodilators

A

For angina, ACS, acute + severe hypertension and oedema

ed nitroprusside

101
Q

Warfarin

A

Inhibits vit K epoxide reductase

102
Q

Heparin

A

Unfractioned- targets thrombin and factor 10a

103
Q

What are the 3 types of blood flow?

A

Laminar
Turbulent
Single-file

104
Q

What is active hyperaemia?

A

An increase in local blood flow in response to an increase in local metabolic activity

105
Q

Atherosclerosis

A

1) Endothelial injury
2) Lesion develops as a plaque in intima of artery wall- lipid core with fibrous cap
3) Cap calcifies
4) Collagen exposure stimulates thrombus formation

BS (5 decks)

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