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ESA 2 > CVS > Flashcards

CVS Flashcards

0
Q

What are the diastolic murmurs and there respective causes?

A

Early diastolic murmur - aortic/pulmonary incompetence

Mid/late diastolic murmur - mitral/tricuspid stenosis

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1
Q

What are the systolic murmurs and there respective causes?

A

Systolic ejection murmur - pulmonary/aortic stenosis
Pansystolic murmur - mitral/septal incompetence or VSD
Late systolic murmur - mitral valve prolapse

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2
Q

What are the causes of continuous murmurs?

A

Patent ductus arteriosus
Aortic stenosis and regurgitation
Pulmonary stenosis and regurgitation

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3
Q

List the acyanotic defects

A 
Ventricular septal defect
Atrial septal defect
Patent foramen ovale
Patent ductus arteriosus
Coarctation of the aorta
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4
Q

List the cyanotic defects

A 
Tetralogy of fallot
Transposition of the great arteries
Tricuspid atresia
Hypoplastic left heart syndrome
Eisenmengers syndrome
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5
Q

List the 4 defects associated with tetralogy of fallot

A

Ventricular septal defect
Right ventricular hypertrophy
Pulmonary stenosis
Overriding aorta

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6
Q

List the four foetal shunts, what they do and their fates

A

Foramen ovale - RA to LA - fossa ovalis
Ductus arteriosus - pulmonary trunk to aorta - ligamentum arteriosum
Ductus venosus - bypass liver from placenta - ligamentum venosum
Umbilical vein - placenta to baby - ligamentum teres

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7
Q

Describe atrial septation

A

Septum Primum grows down towards endocardial cushion and the osmium primum is the hole before fusion. Just before ostium primum closes ostium secundum opens in septum primum by apoptosis. Septum secundum then grows down and also has a hole in it called foramen ovale

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8
Q

Describe ventricular septation

A

Muscular portion grows up towards endocardial cushions. Hole before joining is primary interventricular foramen. This is filled by the membranous portion

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9
Q

List the factors affecting exchange

A

Area available for exchange - capillary density
Diffusion resistance - nature of barrier, molecules and distance
Concentration gradient

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10
Q

What are the bodies requirements for blood at rest and during exercise?

A

Rest: 5L/min
Exercise: 25L/min

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11
Q

Name 3 organs that must always have blood flow and how much they need

A

Brain (0.75), heart (0.3-1.2) and kidneys (1.2)

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12
Q

What is the perfusion rate?

A

Rate of blood flow

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13
Q

What are the components of the cardiovascular system?

A

Pump - heart
Distribution vessels - arteries
Flow control - arterioles and pre capillary sphincter a
Capacitance - veins

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14
Q

What is the approximate distribution of blood in the cardiovascular system?

A

Arteries/arterioles: 11%
Capillaries: 5%
Heart and lungs: 17%
Veins: 67%

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15
Q

What is the course that blood takes through the bodies vessels?

A

Heart-elastic arteries-muscular arteries- arterioles-metarterioles-capillaries-post capillary venules-venules-medium veins-large veins-heart

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16
Q

Name the main elastic (conducting) arteries and their histological make up

A

Aorta, brachiocephalic, common carotid, subclavian, common iliac, pulmonary arteries
Tunica intima
Tunica media - main feature - 40-70 fenestrated elastic membranes
Tunica adventitia - contain vasa vasorum, lymph vessels and nerve fibres

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17
Q

What makes up the wall of a muscular artery?

A

Tunica intima
Tunica media - main feature - 40 layers of smooth muscle
Tunica adventitia

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18
Q

What is an end artery? Give some examples

A

A terminal artery that supplies all/most of the blood to a body part without significant collateral circulation
Coronary artery, splenic artery and renal artery

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19
Q

How does an arteriole differ from an artery?

A

Arterioles are arteries with a diameter less than 0.1mm. They have only 1-3 layers of smooth muscle in the tunica intima

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20
Q

How do metarterioles differ from arterioles? How does this affect their function?

A

The smooth muscle isn’t continuous - a pre capillary sphincter
These can close to stop perfusion to parts of the capillary bed

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21
Q

What are the 3 types of capillary, how do they differ and where would you find them?

A

Continuous - nervous, muscle, connective tissue, exocrine glands and lungs
Fenestrated - have gaps in endothelium - gut, endocrine glands and renal glomerulus
Sinusoidal - larger with larger gaps - liver, spleen and bone marrow

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22
Q

What are pericytes?

A

Form a branching network on the outside of a capillary. Can divide into muscle or fibroblasts during angiogenesis, growth or tumour formation

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23
Q

How are capillaries adapted for exchange?

A

Thin endothelium (1 layer)
Large SA
Narrow so RBCs fill lumen reducing diffusion distance
Lowest blood velocity

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24
Q

How does the structure of a post capillary venule differ from a capillary and a venule?

A

Similar to capillary but more permeable cell wall so fluid drains into it
Venules have smooth muscle (tunica media)

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25
Q

How can you tell a vein apart from its corresponding artery?

A

Larger diameter, thinner wall, more connective tissue and fewer elastic/muscle fibre

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26
Q

What are vena comitantes and where might you find them?

A

Paired veins that accompany an artery

Brachial, ulnar and tibial

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27
Q

Name the large veins and distinguishing features

A

Vena cavae, portal vein, pulmonary vein, renal vein, internal jugular vein, ilial vein and azygous vein
Longitudinal smooth muscle in tunica adventitia, circular smooth muscle in tunica media

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28
Q

What are the distinguishing features of cardiac muscle?

A

Striation, branching, 1-2 central nuclei, intercalated discs, T-tubules in line with Z bands

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29
Q

Define systole and diastole

A

Systole - period when myocardium is contracting

Diastole - relaxation in between contractions

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30
Q

Outline the spread of excitation

A

SAN fires action potential which spreads over the atria causing atrial systole. The action potential reaches the AVN where it is delayed for 120ms before spreading down the septum then from the inner (endocardial) to outer (epicardial) layer. The ventricles will contract from apex up

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31
Q

How is ventricular muscle distributed?

A

In figure of 8 bands that squeeze ventricles effectively contracting apex first

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32
Q

What are the differences between the left and right side of the heart?

A

Left - thicker myocardium

Right - SAN

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33
Q

When and why do the semilunar valves open and close?

A

Open in systole due to intraventricular pressure rising above the pressure in the arteries.
Close at the end of systole when arterial pressure is higher than intraventricular pressure and back flow of blood closes them

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34
Q

When and why do the AV valves open and close?

A

Open in early diastole when pressure in ventricles is lower than atrial pressure.
Close in systole by back flow of blood

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35
Q

Explain the 4 heart sounds

A

S1 - lup/lub - AV valves close
S2 - dup/dub - semilunar valves close
S3 - early diastole
S4 - atrial contraction

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36
Q

Describe the cardiac cycle

A

Early diastole the intraventricular pressure drops below the atrial pressure. Intraventricular pressure drops below arterial pressure at the end of systole and semilunar valves close

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37
Q

What are the borders of the heart?

A

Right - Right atrium
Inferior - Left ventricle
Left - Left ventricle and left atrium
Superior - Right atrium, left atrium and great vessel
Anterior - Right ventricle
Diaphragmatic - Left ventricle and part of right ventricle

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38
Q

What is the function of the pericardium?

A

Fix the heart in the mediastinum
Limit motion
Prevent overfilling - relatively inextensible fibrous layer
Protect from infection by acting as a physical barrier

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39
Q

What layers make up the pericardium from outside to inside?

A

Fibrous

Serous - parietal, pericardial cavity, visceral

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40
Q

What innervated the pericardium?

A

Phrenic nerve C3-C5

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41
Q

What is an aortic dissection?

A

A tear in the inner wall of the aorta. Blood may flow into the wall and cause constriction of the aorta

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42
Q

Explain an aortic aneurysm

A

The aorta dilates >50% its normal diameter due to an underlying weakness such as Marfans disease or an aortic dissection. The main risk is that it could rupture which can rapidly cause death

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43
Q

How are AV valves attached to the heart wall?

A

Papillary muscles attached to the Chordae Tendonae attached to the valve

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44
Q

What is the triangle of Koch?

A

Made up of coronary sinus, tricuspid valve and tendon of todaro
Used to find the AVN

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45
Q

List all the layers of the heart wall from inside to outside

A 
Endocardium - like endothelium
Sub endocardial layer - contains Purkinje fibres
Myocardium - cardiac muscle
Epicardium/visceral layer
Space
Parietal layer
Fibrous pericardium
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46
Q

Explain endocarditis

A

Inflammation of the endocardium, usually on the valves. Clumps “vegetation” develop on the valve and cause inflammation which damages the endocardium and also makes reinfection more likely
Main type - infective endocarditis - vegetation caused by bacteria
Non infective - vegetation caused by something else like malignant cancer

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47
Q

Explain myocarditis

A

Inflammation if the heart muscle
Usually due to adenovirus or Coxsackie B
Symptoms - chest pain, shortness of breath and tachycardia
Result - syncope, arrhythmia and heart failure

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48
Q

Explain a myocardial infarction

A

Myocardium suffers ischaemic damage due to blockage of coronary arteries which is usually due to an atheroma
NSTEMI - Non S-T elevated MI - partial blockage and damage to partial thickness of myocardium
STEMI - S-T elevated MI - complete block and damage to full thickness of myocardium

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49
Q

Explain angina

A

Chest pains due to temporary lack of O2 to myocardium due to narrowed arteries which are usually due to atheroma.
Stable - pain comes on when exercising or during stress
Unstable - pain doesn’t require exertion
Treat with glyceryl trinitrate spray

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50
Q

What is 1st degree heart block?

A

P-R interval over 0.2 seconds

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51
Q

What is type 1 second degree heart block?

A

PR interval lengthens each time and eventually skips a QRS complex. Usually a problem with the AVN

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52
Q

What is type 2 second degree heart block?

A

A constant PR interval but not all P waves will be followed by a QRS complex. Usually a problem with the bundle of His

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53
Q

What is 3rd degree heart block?

A

Normal atrial contraction but electrical activity doesn’t spread to ventricles so have to use ectopic pacemakers. Regular PP interval and RR interval but no correlation between the two. Usually due to coronary ischaemia

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54
Q

Explain left/right bundle branch block

A

Signal not carried by respective branch so excitation spreads from opposite ventricle causing wider QRS interval. Left also has inverted t waves

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55
Q

Explain atrial fibrillation

A

Disorganised electrical impulses overwhelm the SAN resulting in fast and uncoordinated atrial contraction. The AVN prevents severe tachycardia
No P waves
Irregular irregular rhythm
Not much decrease in CO but turbulent blood flow so a stroke risk

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56
Q

Explain ventricular fibrillation

A

No coordinated contraction of the ventricles so results in a big loss of cardiac output. Usually due to a myocardial infarction

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57
Q

Explain ventricular ectopic beats

A

Ventricular cells gain pacemaker activity and cause contraction. Will contain wider and taller QRS complex in ECG

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58
Q

What are some medical procedures used for coronary heart disease?

A

Angiogram
Angioplasty possibly followed by stent insertion
Coronary artery bypass graft

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59
Q

What does the right coronary artery supply and what drains the blood away?

A

RA and RV

Small cardiac vein and middle cardiac vein

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60
Q

What does the right marginal artery supply and what drains the blood away?

A

RV and apex

Small and middle cardiac vein

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61
Q

What does the posterior interventricular artery supply and what drains the blood away?

A

RV, LV and IVS

Left posterior ventricular vein

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62
Q

What does the left coronary artery supply and what drains the blood away?

A

LA and LV

Great cardiac vein

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63
Q

What does the left anterior descending artery supply and what drains the blood away?

A

RV, LV and IVS

Great cardiac vein

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64
Q

What does the left marginal artery supply and what drains the blood away?

A

LV

Left marginal vein and great cardiac vein

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65
Q

What does the left circumflex artery supply and what drains the blood away?

A

LA and LV

Great cardiac vein

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66
Q

What is a cardiac tamponade?

A

Also known as a pericardial effusion
Accumulation of blood or pus in the pericardial cavity
Compressed and ineffective heart
Symptoms - hypotension, raised JVP and muffled heart sounds

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67
Q

What is pericardiocentesis?

A

A procedure to drain fluid in a cardiac tamponade

Needle inserted into left 5/6th intercostal space

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68
Q

What is pericarditis?

A

Chest pain
ST elevation
Rough serous layer which sounds like silk rustling

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69
Q

Outline foetal circulation

A

Placenta to foetus via umbilical vein
Foetus to inferior vena cava by ductus venosus
Right atrium to left atrium by foramen ovale
Left atrium to aorta (pulmonary trunk to aorta by ductus arteriosus)
Then pumped around the body and back to the placenta

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70
Q

How is the primitive heart tube formed?

A

Lateral folding creates the heart tube and cephalocaudal folding brings it into the thoracic region

71
Q

What are the sections of the primitive heart tube from the cranial end to the caudal end?

A 
Aortic roots
Truncus arteriosus
Bulbus cordis
Ventricle
Atrium
Sinus venosus
72
Q

How is the primitive heart tube folded? And what does is accomplish?

A

Bottom - up, left, back
Top - down, right, forward
Inflow is now behind the outflow, both inflow and outflow are at the cranial end and the transverse pericardial sinus has formed

73
Q

How are the atria formed?

A

Right atrium - mainly from primitive atrium and also from the right horn of the sinus venosus
Left atrium - partially from the primitive atrium and also absorbs the proximal parts of the pulmonary veins

74
Q

What does the 4th aortic arch turn into?

A

Right - proximal part of right subclavian artery

Left - arch of aorta

75
Q

What does the 6th aortic arch form and what innervates it?

A

Right - right pulmonary artery
Left - left pulmonary artery and ductus arteriosus
Recurrent laryngeal nerve

76
Q

Explain Eisenmenger syndrome

A

Chronic left to right shunting can lead to vascular remodelling of the pulmonary circulation and an increase in pulmonary resistance. If the resistance of the pulmonary circulation increases beyond that of the systemic circulation the shunt will reverse direction as pressures on the right side of the heart increase (Eisenmenger Syndrome).

77
Q

What are the sympathetic and parasympathetic receptors for: the heart, airway, pupil and sweat glands?

A 
Heart:B1/M2
Airways:B2/M3
Pupil:A1/M3
Sweat:A1 local
M3 general
78
Q

What receptor does adrenaline bind to, what G protein is it and what is the effect?

A

Beta adrenoceptors
Gs
Stimulate adenylyl cyclase

79
Q

What receptors does acetylcholine bind to, what G proteins are used and what are the effectors?

A

M3-Gq-stimulate phospholipase C

M2-Gi-reduce adenylyl cyclase

80
Q

For the adrenoceptors, what is the corresponding G protein and what is the effect?

A

A1 Q +phospholipase C
A2 I -adenylyl cyclase
B1 S +adenylyl cyclase
B2 S + adenylyl cyclase

81
Q

For the muscarinic receptors what is the G protein and what is the effect?

A

M1 Q +phospholipase C
M2 I -adenylyl cyclase
M3 Q +phospholipase C

82
Q

How is the change in blood vessels diameter controlled?

A

Sympathetic nervous system acts on A1 adrenoceptors to make the smooth muscle constrict

83
Q

How is heart rate initially increased?

A

By decreasing the parasympathetic stimulation
Followed by increasing sympathetic which also increases force of contraction
Adrenaline can also act

84
Q

What are chromaffin cells?

A

Specialised sympathetic postganglionic neurones that release adrenaline

85
Q

What are the effects of the sympathetic and parasympathetic nervous system on the pacemaker slope?

A

Sympathetic makes it steeper

Parasympathetic makes it less steep

86
Q

What blood vessels have sympathetic receptors other than A1 adrenoceptors and what is the effect?

A

Skeletal muscle and myocardium have B2 adrenoceptors for adrenaline which causes vasodilation

87
Q

What is the role of local metabolites?

A

Active tissues produce metabolites such as K+, H+, CO2 and adenosine which have a strong vasodilator effect

88
Q

What is the resting membrane potential in cardiac muscle and what is it mainly due to?

A

-90mV

Permeability to K+

89
Q

Describe an action potential in ventricular cells

A

Diastole - resting membrane potential at -90mV
Depolarisation due to electrical activity from SAN which opens fast voltage gated Na+ channels when it reaches the threshold causing further depolarisation
Repolarise back to 0mV by outflow of K+
Na+ channels deactivate but depolarisation has opened voltage gated Ca2+ channels which prolongs depolarisation and also causes CICR
Ca2+ channels close and K+ efflux brings back to resting potential

90
Q

Describe an action potential in pacemaker cells

A

Spontaneous, gradual depolarisation of the cell by slow Na+ channels (funny current)
At threshold Ca2+ channels open
Ca2+ channels close and cell repolarises by K+ efflux

91
Q

List 3 causes of arrhythmia

A

Ectopic pacemaker activity
After depolarisation
Re entry loop

92
Q

What are the 4 types of anti arrhythmic drugs?

A

1 Na+ channel blocker
2 Beta adrenoceptors antagonist
3 K+ channel blockers
4 Ca2+ channel blockers

93
Q

Give an example of a type 1 anti arrhythmic drug and explain how it works

A

Lidocaine
Binds to open or inactivated Na+ channels only
Won’t stop normal action potentials but prevents rapid firing

94
Q

Give an example of a type 2 anti arrhythmic drug and explain how it works

A

Propranolol or atenolol

Blocks sympathetic stimulation, and delays AVN conduction to slow heart. Used after MI to decrease hearts oxygen demand

95
Q

Give an example of a type 3 anti arrhythmic drug and explain how it works

A

Amiodarone

Not normally used as can be pro arrhythmic but this treats Wolff-Parkinson-Whit tachycardia

96
Q

Give an example of a type 4 anti arrhythmic drug and explain how it works

A

Verapamil

Decrease steepness of pacemaker cells slope, reduce AVN conduction, decrease contraction force and vasodilation

97
Q

What is adenosine?

A

Act on A1 (not alpha 1) receptors at the AVN to increase K+ conductance causing hyperpolarisation

98
Q

What is an ionotropic drug? When would a negative and positive ionotropic drug be used?

A

A drug that affects the force of contraction of the heart
-ve used to reduce workload such as after MI e.g. Beta blockers
+ve make heart beat harder such as if patient goes into shock e.g. Dobutamine

99
Q

What are ACE inhibitors and how do they work?

A

Angiotensin converting enzyme inhibitors stop angiotensin I being converted to angiotensin II. Angiotensin II increases Na+ and water reabsorption and is also a vasoconstrictor so ACE inhibitors cause vasodilation and reduce blood volume lowering BP and preload and workload of heart

100
Q

How do you treat an angina?

A

Reduce the workload with beta blockers, Ca2+ channel blockers or organic nitrates

101
Q

What is the mechanism of action of organic nitrates?

A

React to produce NO2- which is reduced to NO which is a powerful vasodilator. It dilates the veins so less blood returns to the heart so the heart has to work less hard. Also dilates coronary arteries so more oxygen goes to the heart
E.g. Glyceryl trinitrate

102
Q

What drugs would you use to treat a thrombus?

A

Warfarin and aspirin

103
Q

What drugs would you use to treat hypertension?

A

ACE inhibitors, beta blockers, calcium blockers and diuretics

104
Q

How do cardiac glycosides work?

A

Block Na pumps, so there’s more Na in the cell so NCX does less work and therefore there’s more Ca2+ in the cell which increases foce of contraction

105
Q

Define flow

A

The volume of fluid passing a given point per unit time

106
Q

Define velocity

A

Rate of movement of fluid particles along the tube

107
Q

What is the difference between laminar and turbulent flow?

A

Laminar - gradient of velocity from middle (fastest) to the edges (slowest)
Turbulent - due to higher mean velocity the layers of fluid try to move over each other than physics allows, increasing resistance

108
Q

Define viscosity

A

Extent to which fluid layers resist sliding over one another
A higher viscosity has a slower central layer and therefore slower mean velocity. It also means the difference between the centre and the edge is small

109
Q

What affect will changing the diameter have on velocity?

A

Velocity is proportional to the cross sectional area of a tube

110
Q

What effects resistance?

A

Increase as viscosity increases

Decrease as diameter increases to power of 4

111
Q

What are the two main equations for calculating flow?

A

Flow=pressure/resistance

Flow=velocity x area

112
Q

What is the difference in the effect on resistance between vessels in series and parallel?

A

Vessels in series add resistance together R1+R2

Vessels in parallel are lower than any one resistance (R1xR2)/(R1+R2)

113
Q

Why is pressure in the arteries high even though there is low resistance?

A

T overcome the high resistance of the arterioles

114
Q

What is the effect of blood vessels having distensible walls?

A

They get stretched by transmural pressure giving a wider diameter and therefore decreasing resistance and increasing flow.
More pressure means the vessels widen and store blood - capacitance
Also means walls will collapse and blood flow will cease if pressure is too low

115
Q

Define systolic, diastolic, pulse and average pressure

A

Maximum arterial pressure. Affected by total peripheral resistance, cardiac output and stretchiness of arteries
Minimum arterial pressure. Affected by systolic pressure and total peripheral resistance
Difference between systolic and diastolic pressure
Diastole + 1/3 pulse pressure OR 2/3 diastole + 1/3 systole

116
Q

What is total peripheral resistance?

A

Sum resistance of all peripheral vasculature in systemic circulation

117
Q

What forms a dicrotic notch and dicrotic wave?

A

Notch - pressure drop due to back flow of blood

Wave - recoil of blood from closed valve raises pressure

118
Q

What is the vasomotor tone?

A

Continuous level of vasoconstriction in vessels due to sympathetic nervous system

119
Q

Explain reactive hyperaemia

A

When circulation is temporarily cut off a large amount of blood can immediately re-enter as vasodilator metabolites are still produced and not washed away by blood

120
Q

Explain autoregulation

A

More metabolically active tissue produce more metabolites and therefore get the more blood that they need. Couples supply to demand

121
Q

Define central venous pressure and venous return

A

Pressure in retreat veins supplying the heart

Rate of flow or blood back to the heart. This limits cardiac output

122
Q

What is the effect in arterial and venous pressure if you increase total peripheral resistance? And if you decrease cardiac output?

A

Increase arterial and reduce venous pressure

Decrease arterial and increase venous pressure

123
Q

Define end diastolic volume and end systolic volume

Define stroke volume

A

Volume of blood in ventricle at the end of diastole and systole respectively
Difference between the end diastolic/systolic volume

124
Q

What is the relationship between ventricular filling and venous pressure?

A

Increasing pressure increases end diastolic volume. Curved graph (x^2) with volume on x and pressure on y

125
Q

Define preload and afterload

A

End diastolic stretch of myocardium determined by venous pressure
Force necessary to expel blood into arteries

126
Q

What is Starling’s law?

A

More heart fills=harder contractions=more stroke volume
Graph is a (-x^2)
Gradient is contractility - stroke volume for a given pressure

127
Q

What is effect on cardiac output of increasing arterial and venous pressure respectively?

A

Due to baroreceptors increasing arterial pressure lowers cardiac output via the autonomic nervous system
Increasing the venous pressure increases the cardiac output

128
Q

Outline the changes following a meal

A

More gut activity=more metabolites=more vasodilation=less TPR=less arterial pressure and more venous pressure=more heart rate and cardiac output=lower venous pressure and higher arterial pressure

129
Q

What are the changes for exercise?

A

The is a large increase in demand and muscle pumping also forces more blood back. Normal response can’t deal with this as it is the flat on starlings curve. Heart rate increases instead

130
Q

Outline the changes accompanying standing up

A

Blood pools in lower veins=lower central venous pressure=lower cardiac output=lower arterial pressure
Both are lowered up which is bad but baroreceptors detect the fall and increase heart rate and total peripheral resistance
If baroreceptors reflex doesn’t work - postural hypotension

131
Q

Outline the changes from haemorrhage

A

Lower blood volume=lower venous pressure=lower cardiac output=lower arterial pressure
Both fall so baroreceptors increase heart rate and total peripheral resistance = lower venous pressure further which is worse
Treat by venison drifting and blood transfusion

132
Q

What is the effect of having a long term increase in blood volume?

A

More blood=more venous pressure=more cardiac output=more arterial pressure=more blood in tissues=higher total peripheral resistance=higher arterial pressure

133
Q

What are the rules for the signal produced by electrodes in ECGs?

A

Depolarisation towards electrode = up
Depolarisation away from electrode = down
Repolarisation towards electrode = down
Repolarisation away from electrode = up
The size is dependent on how much muscle is depolarised and how directly towards/away from the electrode the signal is travelling

134
Q

What forms the P, Q, R, S and T wave in an ECG?

A 
P - atrial depolarisation
Q - septal depolarisation spreading to ventricle
R - main ventricular depolarisation
S - end of ventricular depolarisation
T - ventricular repolarisation
135
Q

How can you calculate the heart rate using an ECG?

A

300/number of squares between R-R complex

If irregular heart rate use more than one R-R interval

136
Q

What are the two circulations to the lungs and the differences between them?

A

Bronchial - systemic circulation to meet metabolic demands of lungs
Pulmonary - circulation to alveoli for gas exchange - low resistance due to short wide vessels, lots of capillaries in parallel and little smooth muscle in the arterioles

137
Q

What are the average pressures found in the pulmonary circulation?

A

Pulmonary artery - 12-15mmHg
Pulmonary capillaries - 9-12mmHg
Pulmonary veins - 5mmHg

138
Q

How is ventilation and perfusion in the alveoli matched?

A

The ventilation perfusion ratio (ideally 0.8) is maintained by diverting blood from poorly ventilated alveoli by hypoxic pulmonary vasoconstriction. If chronic, can cause right ventricular failure

139
Q

How is tissue fluid formed?

A

Starlings forces - hydrostatic pressure of blood in capillaries pushes fluid out and on optic pressure from large molecules in the blood like plasma proteins draws it back in.
Hydrostatic pressure increase can cause an oedema
Fluid accumulates at the base of lungs due to gravity and increased hydrostatic pressure

140
Q

What is the relationship between mechanical work and O2 demand/blood flow in the heart?

A

Almost linear between work and blood flow but at very high demand flow doesn’t increase but oxygen extracted from blood does

141
Q

How is the heart supplied with blood?

A

The right and left coronary arteries arise from the right and left aortic sinuses which fill during diastole.
Cardiac muscle has a high capillary density and continuous production of NO and other metabolites ensures a high flow.
Coronary arteries are end arteries that are prone to atheroma. I they narrow you can get angina on exercise, cold or stress

142
Q

How is the brain adapted to get oxygen?

A

Cerebral circulation has high capillary density (large surface area and short diffusion distance), high basal flow rate and high oxygen extraction.
Secure flow is needed - anastomoses, myogenic autoregulation (for hypotension), metabolic factors and the fact the brain stem regulates other circulations ensures this

143
Q

What is myogenic autoregulation?

How do metabolic factors regulate blood flow?

A

When BP goes up cerebral vessels vasoconstrict. The opposite is also true
Very sensitive to PCO2 - if it increases vasodilation (hyperventilating)
More active areas have increased flow as they produce adenosine a vasodilator

144
Q

What is Cushing’s reflex?

A

The cranium is rigid and can’t expand so increased pressure impairs flow
Cerebral BP increases = peripheral vasoconstriction = more flow to brain

145
Q

How is the blood flow to the skin adapted?

A

Blood flow to the skin is mainly through arterio-venous anastomoses, not capillaries
Important in temperature regulation
Sympathetic innervation decreases blood flow by vasoconstriction

146
Q

How is blood flow to skeletal muscles adapted?

A

The blood flow to skeletal muscle must be able to increase a lot. This is done by opening more capillaries if needed via vasodilator nervous activity and local metabolites. At rest approximately half the capillaries are open

147
Q

What are some possible causes of chest pain?

A

Lungs - pneumonia
GI - peptic ulcer
Chest wall - rib fracture
CVS - angina, MI, pericarditis, aortic dissection

148
Q

Name the modifiable risk factors for ischaemic heart disease

A

Most important - Hyperlipidaemia, smoking, hypertension, diabetes

Exercise, obesity stress

149
Q

What are the non modifiable risk factors for ischaemic heart disease?

A

Age
Gender
Family history

150
Q

How is angina chest pain described?

A

Central, retrosternal, left sided

Crushing

151
Q

Describe stable angina, what causes it and how you would treat it

A

Atheromatous plaque build up occluding over 70% of the coronary artery
Mild to moderate, brief pain, brought on by exertion/cold
Treat with nitrate spray, beta blockers, ACE inhibitors, aspirin, statins and Ca2+ blockers

152
Q

How does an unstable angina differ to a stable angina?

A

Due to further occlusion

More severe pain that occurs at rest or with minimal exertion. Crescendo pattern of occurrence

153
Q

How does a myocardial infarction occur?

A

Complete occlusion of artery leading to death of the myocardium
The fibrous cap of atheromatous plaque is eroded and exposes the blood to underlying thrombogenic material in necrotic core. Thrombus forms (can get embolism)
Severe pain, not relievable, breathless, faint, sense of impending death, sweat, pale, nauseous

154
Q

What are the two types of myocardial infarction and how do they differ?

A

NSTEMI - no ST elevation, infarct isn’t full thickness

STEMI - ST elevation, infarct is full fitness

155
Q

How do diagnose angina?

A

History - risk factors (hypertension, corneal arcus, peripheral vascular disease)
Exercise stress test - exercise until target heart rate reached, chest pain, ECG change (ST elevation > 1mm) or some other problem

156
Q

How do the following differ between an unstable angina, NSTEMI and STEMI: occlusion, necrosis, ECG and biochemical markers

A

Partial/partial/total
None/some/lots
ST depression, T inversion, normal/ST depression, normal/ST elevation
None/some/more (troponin)

157
Q

How would you tell an unstable angina, NSTEMI and STEMI apart?

A

ECG to tell STEMI from NSTEMI and unstable angina

Check for bio markers to tell NSTEMI from unstable angina

158
Q

What bio markers would you look for when diagnosing a MI?

A

Cardiac troponin I/T appear after 3-4 hrs and peak at 18-36 hrs then decline slowly
Creatine kinase MB appears after 3-8 hrs, peaks at 24 hrs and then returns to normal in 48-72 hrs

159
Q

How do you treat an MI or UA?

A

Stop UA progressing to MI
Limit MI muscle loss
Anti-thrombotic - aspirin/heparin
Restore perfusion - angioplasty, coronary artery bypass graft
Pain control, O2, nitrates, beta blockers, statins, ACE inhibitors

160
Q

Describe the following surgical interventions: angiograph, percutaneous coronary intervention, coronary bypass grafting.

A

Inject dye to see vessel occlusion
Angioplasty - inflate balloon inside occluded vessel with mesh to hold it open
Take an artery (mammary, radial, saphenous vein) and graft to heart

161
Q

What are the causes and symptoms of pericarditis?

A

Infections (viral/TB), post MI, surgery, autoimmune, uraemia, malignant deposits
Pain that is worse when inspiring and improved by leaning forward

162
Q

Define heart failure

A

A state in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure

163
Q

What are some likely causes of heart failure?

A

Ischaemic heart disease
Hypertension
Arrhythmia

164
Q

What are the differences between classes I-IV of heart failure?

A

I - No limitation of physical activity
II - Slight limitation of physical activity. Symptoms appear whilst exercising but not at rest
III - Marked limitation of physical activity. Symptoms appear after minor exercise but not at rest
IV - Inability to do any physical activity without symptoms which are also present at rest

165
Q

What are the types of heart failure?

A 
Left sided heart failure
Right sided heart failure
Congestive cardiac failure
Systolic heart failure
Diastolic heart failure
166
Q

What are the differences between the symptoms that appear in left sided heart failure and right sided?

A

Left - pulmonary crackles, SOB, cardiomegaly, mitral regurgitation
Right - pitting oedema, raised JVP, hepatic enlargement/ascites

167
Q

Outline the renin-angiotensin-aldosterone-system

A

Drop in blood pressure causes the kidneys to release renin which converts angiotensin into angiotensin I. ACE then converts angiotensin I into angiotensin II which is a vasoconstrictor and also causes the release of aldosterone which in turn raises blood volume

168
Q

What are the main drugs you would give to treat a patient with heart failure?

A

ACE inhibitors
Diuretics
Beta blockers
(Nitrates, Ca2+ channel blockers! cardiac glycosides)

169
Q

Define shock

A

An acute condition of inadequate blood flow throughout the body caused by a catastrophic drop in arterial blood pressure

170
Q

What are the 4 types of shock?

A

Cardiogenic, mechanical, hypovolaemic and distributive

171
Q

What is cardio genie shock and how might it occur?

A

Ventricle can’t empty properly
Following an MI there is LV damage
Serious arrhythmia
Worsening of heart failure

172
Q

What is mechanical shock and how might it occur?

A

Ventricle can’t fill properly
Cardiac tamponade
Pulmonary embolism

173
Q

What is hypovolaemic shock and how might it occur?

A

A lower blood volume
Haemorrhage - 20-40% blood loss
Burns
Diarrhoea

174
Q

What symptoms might a patient with hypovolaemic shock have?

A

Tachycardia, weak pulse, pale and cold

175
Q

What are the types of distributive shock? Compare and contrast the types

A

Toxic - bacteria release endotoxins which are powerful vasodilators. Tachycardia, warm and red extremities
Anaphylactic - release of histamine or other powerful vasodilation mediators. Difficulty breathing, tachycardia, red and warm extremities
Treat with an epipen

ESA 2 (4 decks)

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