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Y1 Body system lecture notes year 1 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the cardiovascular system

A

The heart and blood vessel make up a blood transportation network response,e for delivering nutrients and oxygen to cells and waste products away from cells

Maintains constant internal environment - homeostasis

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2
Q

What are the two circulations of the CVS

A

Pulmonary: blood from right side of heart to lungs to left side of heart
Systemic: blood from left side of heart to capillary beds to right side of heart

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3
Q

What are the two functional parts of the CVS

A

Conducting: vasculature (tubes)
Exchange: capillary beds

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4
Q

What are the atrioventricular valves

A

Valve between atrium and corresponding ventricle

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5
Q

What are the valves in the heart

A

Tricuspid: RA -> RV
Pulmonary valve
Mitral (bicuspid): LA -> LV
Aortic valve

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6
Q

What is the role of the chord tendineae

A

Keeps the valves from inverting

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7
Q

What are the three parts of the aorta

A

Ascending
Arch
Descending

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8
Q

What branches of the arch of the aorta

A

Brachiocephalic trunk
Left common carotid artery
Left subclavian artery

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9
Q

What does the brachiocephalic trunk branch to form

A

Right common carotid artery

Right subclavian artery

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10
Q

What are the characteristics of the coronary circulation

A

They are the only branches which come from the ascending aorta

Two coronary arteries: left and right

RCA supplies main conducting centres of the heart

Functional end arteries so provide blood to specific areas of the lungs with little overlap

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11
Q

What arteries come from the coronary arteries

A

RCA: right marginal, posterior inter ventricular
LCA: Anterior interventricular, left marginal, circumflex

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12
Q

What would result from a blockage of coronary arteries

A

Reduced/indaquate blood supply
May lead to Ischaemia
Can lead to myocardial infarction

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13
Q

What are the three categories of arteries coming off the descending aorta

A

Ventral, unpaired arteries to GI tract

Paired, arteries to paired internal organs such as kidneys

Paired, segmental arteries to body wall such as intercostal arteries

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14
Q

What does the internal thoracic artery bifurcate into

A

Superior epigastric artery

Musculophrenic artery

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15
Q

At what level does the descending aorta bifurcate

A

L4

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16
Q

What vessels supply and drain from the limbs

A

Upper limbs: subclavian artery; subclavian veins

Lower limbs: external iliac artery; external iliac veins

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17
Q

What is the course of the lymphatic system

A 
Lymphatic plexuses
Lymphatic vessels
Lymph nodes
Thoracic duct or right lymphatic duct
Venous system
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18
Q

What are the tube involved in the lymphatic system

A

Thin wall tubes which transport interstitial fluid, bacteria, cellular debris and whole cells

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19
Q

How is the lymphatic system involved in the spread of carcinomas

A

Lymphogenous

Patterns od lymph flow are important to predict or track back primary tumour

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20
Q

What makes up the body’s circulatory system

A

CVS and lymphatic system

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21
Q

What increases heart rate and decreases heart rate

A

Sympathetic system increases

Parasympathetic stem decreases

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22
Q

What is anatomy vs physiology

A

Physiology: function
Anatomy: structure

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23
Q

How does the vagus nerve act on heart

A

Parasympathetic

Like a brake

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24
Q

What is the sinoatrial node

A

Superior region of right atrium
Region where electrical impulses originate
Spontaneously depolarise
Dominant pacemaker cells

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25
Q

How do electrical impulses move through the heart

A

Start in SA node ->
Propagate through anterior, middle and posterior bundles -> depolarise across both left and right aria which is reflected -> delay at AV node to allow atria to fully contract -> Down through bundle of His which splits into left and right bundle and then into purkinje fibres -> propagates around the whole heart

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26
Q

What does the P wave reflect

A

Depolarisation from SA node through anterior, middle and posterior bundles, across the left and right atria

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27
Q

How do impulses spread quickly

A

Through gap junctions

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28
Q

What is the membrane threshold potential of pacemaker cells

A

-35 mV

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29
Q

What are the differences between pacemaker cells and non-pacemaker cells

A

Non-pacemaker resting potential is more negative: -90mV vs -70mV

NP influx mediated by sodium rather than calcium

NP has a plateau fase mediated by calcium

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30
Q

How is an electrical impulse interpreted from an ECG

A

Electrical activity TOWARDS an electrode gives POSITIVE deflection

Electrical activity AWAY from an electrode gives a NEGATIVE deflection

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31
Q

Where do the V1 to V6 chest leads look

A

V1 and V2 look at right
V3 and V4 look at ventricle septum
V5 and V6 look at left

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32
Q

What is the P-Q interval

A

AV node delay

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33
Q

What is the S-T segment

A

time between depolarisation and re-polarisation of the ventricles

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34
Q

What is the T wave showing

A

Ventricular re-polarisation

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35
Q

What is a sinus arrhythmia

A

Slowing go the SA node rate during expiration caused by an increase in vagal activity

tachycardia on inspiration
bradycardia on expiration

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36
Q

What is sinus bradycardia and what causes it

A

less the 60 beats per minute where mediated by only SA node

Athletic
Sleep
Medications
Hypothyroidism

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37
Q

What is sinus tachycardia and what causes it

A

More the 100 beats per minute where mediated by SA node only

Trauma
Stress response
Hyperthyroidism
Infection
Exercise 
Medication
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38
Q

What is ectopy

A

An extra heartbeat

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39
Q

How is complete heart block picked up on ECG

A

No association between P wave and QRS

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40
Q

What is atrial fibrillation

A

Electrical activity is irregular in atria

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41
Q

What is ventricular fibrillation

A

Electrical activity is irregular in ventricles

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42
Q

What is QRS complex

A

represents depolarisation of the ventricles

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43
Q

What is the PR interval

A

represents time take for electrical activity to move between atria and ventricles

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44
Q

How long does one cycle last

A

0.8 seconds

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45
Q

What is diastole

A

Filling of the heart ventricles

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46
Q

What is systole

A

Contraction of myocardium and ejection of blood

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47
Q

What is the stroke volume and what is the typical resting value

A

Volume of blood ejected from the left ventricle with each cardiac cycle

70ml

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48
Q

What is the cardiac output, what is the typical resting value and how is it calculated

A

Volume of blood ejected from the left ventricle each minute

5.0 l/min

Cardiac output = Heart rate x stroke volume

CO = HR x SV

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49
Q

When does formation of the heart begin

A

Week 3

50
Q

What are the three layers of the heart and where does it derive from

A

Epicardium: visceral layer of the pericardium and derives from the visceral mesoderm

Myocardium: muscular wall; derived from the visceral mesoderm overlying the heart tube

Endocardium: internal endothelial lining of the heart; derived from the heart tube

51
Q

What happens in vasculogenesis

A

Endoderm induces some cells of overlying visceral/splanchnic mesoderm to differentiate into angioblasts which further differentiate into endothelial cells and form tubes which are endocardial tubes

52
Q

How is the primitive heart tube formed

A

Endocardial tubes fuse during lateral folding to form the primitive heart tube

53
Q

How is myocardium made and what is it

A

The visceral mesoderm surrounding the primitive heart tube differentiates to form the myocardium which is the heart muscle and it secrets a thick layer of extracellular matrix which is cardiac jelly

54
Q

What does the cranio-caudal folding cause for the heart

A

Brings the heart tube into the thorax

55
Q

What are the five dilations of the heart tube

A 
Truncus arteriosus (bulbous cordis)
Conus arteriosus (bulbis cordis)
Primitive Ventricle
Primitive Atrium
Sinus venosus
56
Q

What happens on day 23

A

The heart tube begins to fold in preparation of forming the four chambers of the heart

Bulbus cordis: moves caudally, centrally and to the right

Primitive ventricle: displaced before moving back to midline

Primitive atrium: displaces cranially and dorsally

57
Q

How are the ventricles formed

A

Majority of from primitive ventricle (trabeculated/rough)

and some from the conus arteriosus (smooth)

58
Q

What does the right horn of the sinus venosus form

A

Sinus venarum (smooth part)

59
Q

What landmark separated the smooth and rough parts of the atrial wall

A

Crista terminalis

60
Q

Which layer of the heart tube forms the coronary arteries

A

Epicardium

61
Q

What is intussusception and when does this happen

A

The 4 pulmonary veins are incorporated into the wall of the left atrium
Week 5

62
Q

How is the primitive atrium separated and when does this happen

A

A crescent-shaped outgrowth from the dorsal wall forms called the septum primum and extends to diminish the connection between left and right sides

63
Q

How is the atrioventricular septum formed

A

The endothelium lining the boundary between the atrium and ventricle expands to form dorsal and ventral endocardial cushion which fuse together to form the AV septum

64
Q

How is the foramen secundum formed

A

Apoptosis occurs in the upper part of the septum premium to form a hole

65
Q

What is the foramen ovale

A

An opening in the septum secundum which is formed at the same time as the foramen secundum

It allows the blood to flow from the right atrium to the left atrium, bypassing the lungs

66
Q

How is the primitive ventricle separated and when does this happen

A

End of week 4
The muscular part that projects from the floor of the primitive ventricle towards the endocardial cushion leaving an inter-ventricular foramen

Week 7
A membranous part the projects inferiorly from eh endocardial cushion to close the inter-venticular foramen

67
Q

What happens to the trunks arteriosus

A

Separation into aorta and pulmonary trunk

Divided into 2 channels by endocardial swellings (conotruncal ridges)

Swellings fuse to form a septum (conotruncal septum) that separates the outflow of left and right ventricles and fuses with the inter ventricular septum

The conotruncal swellings don’t fuse in a straight line but spiral around each other

68
Q

What’s the difference in foetal circulation

A

Mother’s circulation is oxygenating and detoxifying blood therefore the foetal circulation shunts blood away from the lungs and liver

69
Q

What is dextrocardia

A

Heart points towards the right side of chest instead of the left
May be a result of abnormal cardiac looping a=or induced during gastrulation (week 3)

70
Q

What is patent ductus arteriosus

A

Ductus arteriousus doesn’t close at birth and so blood is shunted from aorta back into pulmonary trunk

71
Q

What causes atrial septal defects

A

Failure of the septum premium and secundum to fuse after both

Malformations in the septum premum or secundumsuch that they do not overlap and therefore leave a gap

72
Q

What is the premature closing of foramen ovale

A

Closure of foramen ovale during prenatal life

Results in hypertrophy of the right side of heart and underdevelopment of the left side

73
Q

What is ventricular septal defect

A

Most common congenital heart defect
Often associated with the defects
Can affect the muscular or membranous part of the inter-ventricular septum
Defects in muscle often resolve as child ages
Allows left to right shunting blood
Can result in pulmonary hypertension and hypertrophy of right ventricle

74
Q

What are the septation defects of the trunks arteriosus

A

Conotuncal swellings form the septum by migration of neural crest cells from the neural tube and so if they develop abnormally or migrate abnormally, defects occur

Persistant truncus arteriosus
Transposition of the great vessels
Tetralogy of Fallot

75
Q

What is Tetrology of Fallot

A

A collection of four abnormalities with the same primary defect:
Pulmonary stenosis
Ventricular septal defect
Overriding aorta (rightward displacement of aorta)
Right ventricular hypertrophy caused by higher pressure of the right side

Leads to cyanosis: poor oxygenation of the body

76
Q

What are the differences of white and red thrombus

A

White: contains lots of platelets, forms in fast flowing blood
Red: Contains lots of red blood cells, forms in slow flowing blood

77
Q

What makes up a muscle

A

Each muscle is made up of muscle fibre and each muscle fibre is made up of myofibril

Myofibril contains thin filament (actin) and thick filament (myosin)

78
Q

What is the cardiac functional reserve

A

Cardiac reserve refers to the difference between the rate at which the heart pumps blood and its maximum capacity for pumping blood at any given time

Cardiac reserve = maximal cardiac output - cardiac output at rest

79
Q

What are the factors the influence myocardial contractility

A

Increase preload -> increased cardiac performance
Increase after load -> increased contractility
Increase heart rate -> increased contractility

80
Q

Describe molecular biology of muscular contraction and energy generation

A

Tropomyosin and troponin work together to block binding sites on actin
When a calcium ion binds to troponin, the troponin-tropomyosin complex moves, exposing myosin binding sites

The chemical energy stored within ATP is converted into mechanical energy resulting in force generation and myofilament shortening

This transforms basic mechanical energy into useful hydraulic function for the whole organ

81
Q

What are some clinical examples of myocardium decreasing resulting in less contraction

A

Ischemia: scarred myocardium less able to contract

Viral infection/ alcohol: wall thinning

82
Q

How is mean systemic arterial blood pressure calculated

A

Cardiac output x Total peripheral resistance = Mean systemic arterial pressure

83
Q

What increases the preload

A 
Increase:
circulating volume,
Central venous pressure
respiratory pump
atrial filling or contraction

Decrease:
Venous compliance
heart rate

84
Q

What is the Bainbridge reflex

A

Increased venous return
Baroreceptors in the atria detect increased stretch
Heart rate increased via sympathetic stimulation to SA node

Antagonistic to baroreceptor response
Involved in sinus arrhythmia

85
Q

How does the sympathetic nervous system act on the heart

A

+ chronotropy: SA node to speed up to increase heart rate
+ dromotropy: Increase speed of conduction through AV node
+ inotropy: increases force of contraction in ventricles and atria
+ luisitropy: increased relaxation of ventricles and atria

86
Q

What are the actions of the Renin angiotensin system

A

Angiotensin II: vasoconstriction
Increased Na+ and H2O retention

Aldosterone: increased Na+ and H2O retention

Vasopressin (antidiuretic hormone): promotes H2O retention

87
Q

How does the parasympathetic nervous system act on the heart

A
  • chronotropy: decreased heart rate
  • dromotropy: decreased AV conduction
  • inotropy: decreased atrial contractility
    No effect on ventricles
88
Q

What are the barareceptors

A

Located: carotid sinuses, aortic arch
Decrease arterial pressure: decreased firing
Increased arterial pressure- increased firing

Increased baroreceptor firing: decreases sympathetic tone and increases parasympathetic tone

AND THE REVERSE IS TRUE

89
Q

What is blood pressure

A

Driving force propelling blood to tissues
Balance between organ perfusion and vascular damage
Closely auto-regulated

90
Q

What is hypertension

A

BP control mechanisms are dysfunctional or are unable to compensate for stressors on the body

Defined as SBP >/= 140mmHg and/or DBP >/= 90mmHg

91
Q

How is hypertension classified and what causes this

A

Primary: more common, age related or unknown
Secondary: specific cause: renal vascular disease, Cushing’s syndrome, coarctation of aorta, tumour, pregnancy

92
Q

How can cardiac disease present

A 
Stroke, TIA
Heart failure
Arrhythmia
Angina
MI
Renal failure
Aortic aneurysm
Impotence (reproduction)
Mesenteric ischemia/ infarction
Peripheral vascular disease
93
Q

How can hypertension be managed

A

Lifestyle changes
Medication: ace inhibitors (ramipril), Angiotensin II receptor antagonist (candesartan), Aldosterone blockers (Spironolactone) calcium channel blockers, diuretics, beta-blockers

94
Q

What are some contraindications for hypertension medications

A

ACEi -> pregnancy
B blockers -> asthma
Diuretics -> hypokalaemia, gout

95
Q

What is the preload

A

The level of stretch that a cardiomyocyte is exposed to before ventricular ejection

96
Q

What is the afterload

A

The pressure against which the heart is contracting when it ejects blood

97
Q

What is Starling’s law of the heart

A

The law of the heart is thus the same as the law of muscular tissue in general, that the energy of contraction, however measured, is a function of the length of the muscle fibre

98
Q

What is aldosterone

A

Mineralcorticoid
From adrenal cortex
Released in response to Angiotensin II
Renal tubular effects

99
Q

How does aldosterone work

A

Acts on DCT and collecting duct
Internalised and binds to intracellular aldosterone receptor
Increases transcription of gene for epithelial Na+ channels
Augments reabsorption of Na+ and H2O
Excretes K+
Increases Angiotensin II receptors

100
Q

What happens in heart failure

A

Back pressure in LV causes raised pressure in pulmonary circulation
Increased hydrostatic pressure forces fluid outside vascular compartment
Interstitial space in lungs fills with fluid
Pulmonary oedema/ pleural effusions

101
Q

What would be the acute therapy in heart failure

A 
Resuscitation
Airways, Breathing, Circulation (ABC)
Oxygen
Optimise alveolar ventilation
Increase pressure in airways to oxygenate blood
Non-invasive or invasive ventilation
102
Q

Why is morphine given to patients with heart failure

A

Pain management
Relax pulmonary vessels
Reduce her preload and take stain off the LV
Help with her breathing

103
Q

What do diuretics do in patients with heart failure and what are the side effects

A

Limit reabsorption of fluid
Offloads the ventricles
Moves back along the Starling curve
Can maximise LV contractility

Side effects:
Renal dysfunction
Reduces Na, K, Mg
Can induce diabetes

104
Q

How do beta-receptors work

A

Involved in myocardial and renal responses to reduce cardiac output

105
Q

How do beta-blockers work in patients with heart failure and what are the potential side effects

A

Block beta-receptors resulting in decreased heart rate
Moves back along the Bowditch curve
Allows LV more relaxation time, soberer filling
Also blunts RAAS over-activation

Side effects: asthma, low HR, heart blocks

106
Q

What is the main energy supply of the heart

A

Fat as it can burn more ATP per gram but can in theory burn anything

107
Q

What are the characteristics of capillaries

A 
Single layer of endothelial cells
5- 10uM in diameter
0.5-1 mm in length
Blood cell velocity approx 0.3-1mm/sec
Short distance between capillary and cell it serves
Junctions between capillary cells normally tight but very tight in CNS, and large clefts between cells in liver and bone marrow
A large network
Large surface area
108
Q

What are the three types of capillaries

A

Continuous capillary: fat, muscle, nervous system
Fenestrated capillary: intestinal villi, endocrine glands, kidney glomeruli
Discontinuous capillary: liver, bone marrow, spleen

109
Q

What is an oedema

A

An increase in volume of the interstitial fluid above normal

110
Q

What is a stroke

A

The rapidly developing loss of brain function due to disturbances in the blood supply to the brain

111
Q

What is cerebral haemorrhage and how is it prevented

A

Rupture of a blood vessel can produce a bleeding type of a stroke when an aneurysm of a blood vessel in the brain ruptures

By controlling blood pressure

112
Q

What is cerebral ischaemia

A

Blockage of blood vessel

May be due to thrombus or embolus

113
Q

What is a transient ischaemic attack

A

A mini stroke
Result of temporary disruption of the circulation to the part of the brain due to embolism or thrombosis to brain arteries

114
Q

What are the symptoms of a stroke

A

Localised abnormalities of the nervous system:
Weakness in arm or leg
Slurring of speech
Drooping corner of mouth
Difficulty swallowing
Inability to find the right words to say or lack of understanding of words

115
Q

What investigations can be done in stroke patients

A

Brain CT
Ultrasound of carotid artery
Echocardiogram
ECG

116
Q

What is angina

A

Pain in the centre of the chest that may spread to the jaw and arms
Induced by exercise and relieved by rest
Occurs when the demand for blood by the heart exceeds the supply of the coronary arteries
Usually results from coronary artery atheroma

117
Q

What happens during a heart attack

A

Most heart attacks are caused by coronary artery disease where the arteries narrow due to a gradual build-up of artheroma within their walls
If the atheroma becomes unstable, a piece may break off and lead to blood clot forming which can block the coronary artery starving the heart of blood and oxygen causing damage to the heart muscle which is the heart attack

118
Q

What are the other names for a heart attack

A

Acute coronary syndrome
Myocardial infarction
Coronary thrombosis

119
Q

What are the treatment options for aortic stenosis

A

Aortic valve replacement

120
Q

What is myocarditis and what causes it

A

Inflammation of the heart muscle

Infection, immunological causes, drugs and toxins, viral causes

121
Q

What are the symptoms of systolic heart failure

A 
Shortness of breath
Swelling of feet and legs
Chronic lack of energy
Difficulty sleeping due to Breathing problems
Swollen or tender abdomen with loss of appetite
Cough with frothy sputum
Increased urination at night
Confusion and/or impaired memory
122
Q

What is a cardiac synacope

A

The medical term for fainting, a sudden, usually temporary, loss of consciousness generally

Y1 Body system lecture notes year 1 (5 decks)

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