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Y1S2- Cardio, Resp, Loco > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

blood clot/ haemotoma

A

Solidification of blood constituents outside the vascular system or after death

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2
Q

virchow’s triad

A

endothelial injury, abnormal blood flow, hypercoagulability

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3
Q

hypercoagulability-

A

Alteration of the blood coagulation mechanism}} (esp. platelets and clotting cascade) that in some way predisposes to thrombosis

  • May be genetic disposition eg. protein S or C deficiency
  • May be acquired eg. :after surgical procedures
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4
Q

at what point does the primordial heart and vascular system begin to develop?

A

3rd week of gestation

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5
Q

trilaminar discs form

A

skeletal muscles, blood cells, most of CV system

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6
Q

heart fields are

A

cells that go on to from the cardiovascular system

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7
Q

formation of primary heart tube

A

folding of the embryo in the midline (from cranial to caudal) which brings the heart fields together. Endocardial tubes then fold into the midline and fuse to form one, primary heart tube.

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8
Q

Layers of primary heart tube

A
  • Myocardium: walls of the heart, formed from mesoderm containing myocardial progenitors
  • Cardiac jelly- separates the myocardium from the cardiac tube
  • Endocardium- inner lining of the heart
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9
Q

cardiac looping

A

the cardiac tube elongates, and cardiac looping occurs forming 2 bulges: the bulbus cordis and primordial ventricle.

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10
Q

most caudal of primitive heart chambers?

A

sinus venosus

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11
Q

What sources does the blood flow to the sinus venosus of the primitive heart come from

A
  1. Vitelline veins- returning poorly oxygenates blood from the yolk sac
  2. Umbilical veins- carrying oxygenated blood from the chorionic sac
  3. Common cardinal veins- returns poorly oxygenated blood from embryo itself to the heart
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12
Q

what happens when heart tub elongates and loops:

A
  • The primitive atria are displaced dorsally and cranially
  • The primitive ventricles are displaced caudally with the left ventricle to the left and the right ventricle towards the right
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13
Q

cardiac septation

A

myocardium divides and thickens to form dorsal and ventral endocardial cushions which develop into the septa which divides the atria from the ventricles. The interventricular septum grows upwards to separate right and left ventricles joining to the endocardial cushions at around week 8. The mitral valve and tricuspid valve begin to form after septation.

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14
Q

Septum primum forms and grows downwards 

A

foramen primum space formed

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15
Q

Foramen secundum forms in septum primum 

A

septum secundum begins to form

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16
Q

which valves begin to form after septation?

A

mitral valve and tricuspid valve

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17
Q

fetal blood circulation

A

Fetal lungs are not yet functional so oxygen rich blood from chorionic sac/placenta enters RA and goes directly into the LA.

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18
Q

foramen ovale

A

hole in the atrial septa that permits oxygen rich blood to move from RA to LA

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19
Q
  • Patent ductus arteriosus-
A

connection between pulmonary artery and aorta in the fetus remains open after birth

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20
Q

patent foramen ovale –

A

due to abnormal resorption of septum primum during formation of foramen secundum and can result in short septum primum and therefore foramen ovale

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21
Q
  • Transposition of the great arteries
A
  • pulmonary artery and aorta are swapped
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22
Q
  • Truncus arteriosus-
A

pulmonary artery and aorta don’t develop

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23
Q

positioning of heart

A

sits in the midline of the thoracic cavity and the apex of the heart projects left

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24
Q

diastole

A

passive filling of chambers

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25
Q

systole

A

contraction of chambers

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26
Q

features of arteries near heart and in body

A

Muscular- mostly in the rest of body
Elastic- close to heart
Blood vessels decrease in size moving away from the heart and then increase on return to the heart.

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27
Q

capillaries

A

site of diffusion

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28
Q

The arterial system is:

A
  • Relatively low volume, high pressure
  • Low capacity
  • Low compliance walls- resist deformation so doesn’t expand or shrink
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29
Q

the venous system is:

A
  • High volume, low pressure
  • High capacity
  • Walls have increased compliance so stretchy
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30
Q

Capillary beds:

A
  • Site of exchange within interstitial fluid/ tissues
  • Delivers nutrients and collects waste
  • Feeds into venous system, returns to heart
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31
Q

metarteriole

A

network of tiny true capillaries branch from capillary bed

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32
Q

epithelial layer- tunica intima

A
  • Lines inside of the entire vascular system
  • Flattened epithelial cells
  • Supported by connective tissue, basement membrane and collagen
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33
Q

Muscular Layer- Tunica media

A
  • Smooth muscle
  • Thickness highly variable depending on vessel types
  • Absent in blood capillaries
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34
Q

supporting layer- tunica adventitia

A
  • Connective tissues- elastin and collagen

- Carries small blood vessels which supply vessel walls

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35
Q

layer that indicates what vessel it is

A

Muscular Layer- Tunica media, arteries are more well defined

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36
Q

pulmonary circulation

A

Blood exits the right ventricle via pulmonary trunk → divides into L + R pulmonary artery → smaller branches pass into the lungs → blood accumulates oxygen → blood returned via veins which unite to form pulmonary veins → enter left atrium on posterior aspect of heart

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37
Q

systemic circulation

A

Blood returned from body via superior vena cava (SVC) and inferior vena cava (IVC)- higher pressure that pulmonary, deoxygenated blood drains into right atrium

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38
Q

cardiac cycle

A
  1. Flow into atria- continuous except when they contract, inflow leads to pressure rise
  2. Opening of A-V valves- flow to ventricles
  3. Atrial systole- completes filling of ventricles
  4. Ventricular systole (atrial diastole)- pressure rise closes A-V valves, opens semilunar valves (aortic and pulmonary)
  5. Ventricular diastole- causes closure of semilunar valves
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39
Q

heart sounds

A

1st heart sound= closing of AV valves (lub)

2nd heart sound= closing of semilunar valves (dub)

3rd heart sound= early diastole of young and trained athletes, normally absent after middle age, termed the ventricular gallop, re-emergence later in life indicated abnormality (eg. heart failure)

4th heart sound= caused by turbulent blood flow due to stiffening of walls of left ventricle, occurs prior to 1st heart sound, atrial gallop

*In tachycardia, 3+4 indistinguishable= summation gallop

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40
Q

stroke volume is dependant on:

A
  1. Contractility (force of contraction) eg. adrenaline increases force and stroke volume
  2. End diastolic volume (volume of blood in ventricle at the end of diastole)- force is stronger the more muscle fibres are stretched (within limits)
    Frank- Starling Mechanism/ Starling’s Law of the Heart: stroke volume ∝ diastolic filling
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41
Q

Frank Starling Mechanism/ Preload is Important in:

A
  • Ensuring the heart can deal with wide variation in venous return
  • Balancing the outputs of the two side of the heart
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42
Q

what does the elastic arterial tree store?

A

pressure energy which helps maintain pressure in the arterial system during diastole (pressure drops only about a third from systolic BP)

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43
Q

ejection fraction

A

% volume pumped out, between 55 to 60% but can be 80% during exercise, in heart failure it can be 20%

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44
Q
  • stroke volume=
A

volume of blood pumped by each ventricle per beat (difference between 75ml)- may double during exercise

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45
Q

why does systemic arterial pressure remain high during the cardiac cycle?

A

due to elasticity of the vessel walls and peripheral resistance

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46
Q

cardiac output

A
  • volume of blood pumped per minute
  • CO= HR x stroke volume
  • at rest, CO= 5l/min
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47
Q

causes of strokes:

A
  • cerebral infarction
  • cerebral haemorrhage
  • cerebral thrombosis
  • cerebral embolus
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48
Q
  • cerebral infarction
A

blockage of an artery, narrowing of an artery because plaques are taking up space and less oxygen and blood can move through it, can be due to due to thrombosis or embolism

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49
Q

cerebral haemorrhage

A

results reduction of oxygen to a certain part of the brain due to large occlusion of a blood vessel or an aneurysm

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50
Q

cerebral embolus

A

a part of thrombosis can break off and lodge itself somewhere else causing symptoms elsewhere eg. pulmonary embolism

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51
Q

what can thrombosis in the neurovascular bundle in the leg lead to?

A

a pulmonary embolism which can travel through the venous system

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52
Q

The Excitation Path

A
  • Action potential (carried by sodium channels) then activates atria
  • Atrial action potential activates AV node
  • AV node- small cells, slow conduction velocity- introduces delay of 0.1 sec (delays are important to cardiac muscle but not to skeletal muscle)
  • AV node activates bundle of His/ Purkinje fibres
  • Purkinje fibres activate ventricles
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53
Q

sinus rhythm

A

heart rhythm controlled by SA node, rest rate approx.. 72 beats/min (wide variation)

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54
Q

bundle of His

A

Insulated connective tissue between connecting ventricles allows delays to be put into place, electrical insulator.

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55
Q

Cardiac muscle is myogenic-

A

it generates its own action potentials.

- APs develop spontaneously at the sino-atrial node

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56
Q

intercalated discs

A

adhering structures that hold individual cardiomyocytes together to form the functional syncytium that contracts rhythmically

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57
Q

adhering junctions in intercalated discs:

A
  • Fascia adherins- anchor sites for actin
  • Desmosomes- provide structural support and bind cardiomyocytes together to prevent separation
  • Gap junctions- formed from connexins, allow action potentials to pass between cardiomyocytes
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58
Q

what do T tubules in the sarcolemma allow?

A

depolarisation of the membrane to penetrate the muscle fibre

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59
Q

comparison of cardiomyocyte and skeletal T tubules

A

cardiomyocyte T tubules are less prevalent, larger and wider

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60
Q

excitation- contraction couple in skeletal muscle

A
  • Intracellular calcium release from T tubules in the SR
  • Cross bridge formation and muscle contraction
  • Calcium removal by calsequestrin and muscle relaxation
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61
Q

skeletal muscle is neurogenic

A

needs a nervous impulse to initiate a contraction

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62
Q

Action potential controls

A

the duration and force of contraction in the heart. Only acts as a trigger in skeletal muscle.
Increasing the action potential length = increase duration and force of contraction.

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63
Q

Ca induced Ca release

A
  • The SR contains L type calcium channels that are activated in response to electrical stimuli allowing calcium to enter cardiomyocytes
  • Activation also opens calcium-release channels on the SR causing release of its calcium stores
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64
Q

How is uptake of Ca by SR managed:

A

ATP driven Ca pump

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65
Q

Exit of Ca from cell can be through either:

A
  • An ATP driven Ca pump (weak)

- Na-Ca exchange protein (energy from Na entry gradient)

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66
Q

endocrine, paracrine and autocrine hormones

A

Endocrine hormones- acts on distant cells/organs eg. thyroxine, calcitonin, adrenaline, oestrogen, testosterone
Paracrine hormones- acts on adjacent cells/organs eg. nitric oxide, endothelin, noradrenaline
Autocrine hormones- acts on the same cell/organ eg. endothelin, noradrenaline

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67
Q

classical vasoactive hormones in endocrine regulation

A
  • ANGII
  • Aldo
  • noraadrenaline
  • adrenaline
  • arg vasopressin
  • ADH
  • neutretic peptides- atrial, brain
  • others: relaxin, uromodulin, urotensin
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68
Q

renin- angiotensin system

A
  • Kidney is sensor of BP and salt loss
    1. Excess loss of salt or drop in afferent pressure cause juxtaglomerular cells produce renin
    2. Renin travels in the bloodstream and causes the cleavage of angiotensinogen into angiotensin I
    3. ACE further cleaves angiotensin I into angiotensin II
    4. Angiotensin II stimulates the release of aldosterone from the adrenal cortex
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69
Q

function of ANGII

A
  • increases the reabsorption of salt by the PCT (proximal convoluted tubule)
  • activates the sympathetic nervous system centrally
  • Stimulates release of aldosterone from the adrenal cortex
  • Constricts blood vessels
  • Influences ADH secretion
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70
Q

adrenaline effects on body:

A

Adrenaline (adrenal gland): tachycardia, increased cardiac contractility (b1), increased muscle blood flow, bronchodilation (b2), hypertension, ect.

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71
Q

noradrenaline effects on body:

A

Noradrenaline (peripheral neurotransmitter): peripheral vasoconstriction (a1), renal and splanchnic vasoconstriction, hypertension

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72
Q

what are natriuretic peptides? function

A
  • Used as biomarker of heart failure- high end terminal BNP= heart failure
  • Powerful natriuretic and diuretic effect in kidney
  • Block production of renin and reduce production of angiotensin II
  • Dilate blood vessels
  • Rely on stretch receptors in heart
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73
Q

hormones that cause retention and excretion of body sodium

A

retain: ANGII, Aldo
excrete: ANP/BNP

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74
Q

hormones that cause retention and excretion of body water

A

retain: ADH/AVP
excrete: ANP/BNP

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75
Q

hormones that increase/decrease cardiac output

A

inc: AD
decrease: NA

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76
Q

hormones that increase/decrease BP

A

inc: NA, AD, ANGII, Aldo
dec: ANP/BNP

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77
Q

What mediators affect blood vessel tone, BP and kidney function?

A

ANG II/ALDO, Adrenaline, AVP, ADH, ANP/BNP

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78
Q

Overall cause of endothelial dysfunction

A

less NO generation, more ET-1

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79
Q

Nitric oxide generation and action

A

NO generation: L-arginine is converted to L-citrulline by NO synthase which gives off NO
Action: activates guanylate cyclase which produces cGMP which causes smooth muscle cells to relax by reducing availability of calcium

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80
Q

inhibitor of NO generation

A

L-monomethyl arginine

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81
Q

NO function

A
  • Acts primarily on vascular smooth muscle cells
  • Vasodilatory
  • Anti-proliferative
  • Anti-inflammatory
  • Anti- platelet
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82
Q

Endothelin-1 generation and inhibitors

A

Big Endothelin-1 is cleaved by Endothelin Converting Enzyme to form Endothelin-1. This production can be blocked by an ECE inhibitor or an endothelin receptor antagonist

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83
Q

ET-1 functions at ETA receptor

A 
ETA receptor 
• Vasoconstriction
• Hypertension
• Arterial stiffness
• Endothelial dysfunction
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84
Q

ET-1 functions at ETB receptor

A
  • Vasodilatation
  • ET-1 clearance
  • Natriuresis (exertion of sodium in urine)
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85
Q

ideal cardiac biomarker should be:

A

high sensitivity, hifh specificity, rapid release for early diagnosis, cost effective

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86
Q

homocysteine biomarker

A
  • Linked to atherosclerosis through vascular wall damage
  • May be elevated in B-vitamin deficiency: Vit B6, B9 (folate), B12
  • Very high CV risk in individuals with “classical homocystinuria” = autosomal recessive
  • Tends to be measured when CV disease presents in young patients in the absence of usual risk factors
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87
Q

high sensitivity troponin biomarker

A
  • Protein specific to cardiac muscle
  • Established use in diagnosis of myocardial infarction (MI)
  • predict long-term CV risk
  • Appears superior to hsCRP
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88
Q

how is a coronary stent placed?

A

Primary PCI (cardiac catheterisation)

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89
Q

types of CHD

A

angina (chronic), myocardial infarction (acute)

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90
Q

ACS- acute coronary syndrome: causes, presentation, types

A
  • Myocardial infarction is a cause of the clinical presentation of ACS
  • Presents with chest pain/ discomfort
  • Caused by acute ischaemia, secondary to coronary heart disease

ACS includes:
• acute MI (STEMI, NSTEMI) – significant myocardial damage
• unstable angina – acute symptoms, but no significant tissue damage

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91
Q

why is cardiac troponin a good cardiac biomarker?

A
  • Rapid response
  • Sensitive – capable of detecting “smaller” Mis
  • Best specificity for cardiac tissue
  • Suitable for late presentation
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92
Q

troponin complex

A

1:1:1 complex of three regulatory proteins (TnT, TnI, TnC), exclusively present in striated muscle
• regulates the interaction between actin and myosin
• cardiac specific forms- cTnI, cTnT

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93
Q

what is detectable in those without myocardial damage?

A

• hsTnI, hsTnT

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94
Q

thresholds for acute MI (men and women)

A

34 ng/L for men, 16 ng/L for women

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95
Q

heart failure definition

A

clinical syndrome in which the heart is unable to maintain a cardiac output (CO) that satisfies the metabolic demands of the body

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96
Q

BNP and NT-proBNP in blood during heart failure

A

Levels of both in your blood go up when your heart failure gets worse and go down when it gets better.

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97
Q

atheroma

A

plaques found in elastic and medium-large muscular arteries

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98
Q

risk factors of atheroma

A
  • Age
  • Male sex
  • Genetics
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Diabetes mellitus
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99
Q

Arteries that atheromas can form in

A

Elastic and medium-large muscular arteries:

  • Abdominal aorta
  • Coronary arteries
  • Popliteal arteries
  • Descending thoracic aorta
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100
Q

thrombus definition

A

solidification of blood constituents that form within the vascular system during life

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101
Q

complications of atheroma

A
  • Calcification
  • Ulceration
  • Thrombosis
  • Plaque rupture
  • Haemorrhage
  • Aneurysmal dilation- localised swelling caused by weakening of walls
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102
Q

histological appearance of thrombus

A

alternating pale and dark lines of Zahn

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103
Q

arterial thrombi properties

A
  • Usually occlusive
  • May be mural- adhere to wall of artery
  • Frequent in coronary, carotid cerebral and femoral arteries
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104
Q

where do venous thrombi usually occur?

A

Occurs typically in pelvis and leg veins in association with stasis

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105
Q

complications of thrombosis

A
  • Occlusion of artery or vein: area becomes cold, pale, painful and eventually tissue dies & gangrene
  • Embolism
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106
Q

deep and superficial venous thrombosis- symptoms

A

Superficial (saphenous)- congestion, swelling, pain, tenderness (rarely embolise)
Deep- foot and ankle oedema, may be asymptomatic and recognised only when they have embolised (to lung)

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107
Q

embolus definition

A

detached intravascular solid, liquid or gaseous mass that is carried by blood to a site distant from its point of origin

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108
Q

Less common/rare forms of emboli include fragments of:

A
  • Bone or bone marrow
  • Atheromatous debris
  • Droplets of fat
  • Foreign bodies (like bullets)
  • Bubbles of air or nitrogen
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109
Q

types of embolism

A
  • Pulmonary embolism
  • Systemic embolism
  • Amniotic fluid embolism
  • Air embolism
  • Fat embolism
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110
Q

common origins of pulmonary embolisms

A

thrombi within large deep veins of lower leg or pelvic veins

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111
Q

actions of different sized pulmonary emboli

A
  • Large emboli may impact the main pulmonary artery or lodge at the bifurcation as a saddle embolus
  • Causes circulatory obstruction and are associated with collapse and sudden death
  • Smaller emboli can travel out into the more peripheral pulmonary arteries
  • If of intermediate size, they may cause pulmonary infarction particularly in patients with cardiac failure
  • If very small and recurrent, may lead to pulmonary hypertension
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112
Q

paradoxical embolism

A
  • In presence of interatrial or interventricular defect they may gain access to the systemic circulation
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113
Q

microscopic appearance of emboli

A

same as thombi

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114
Q

pulmonary embolism and infarction

A
  • Pulmonary infarction is typically haemorrhagic
  • Base of the infarct faces the pleural surface
  • Patients may therefore present with haemoptysis (coughing up blood) and/or chest pain (pain on inspiration)
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115
Q

infarct

A

area of ischaemic necrosis caused by occlusion of arterial supply or venous drainage in a particular tissue

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116
Q

5 causes of infarction

A
  • Thrombosis and thromboembolism account for vast majority
  • Vasospasm
  • Expansion of atheroma
  • Compression of vessels
  • trauma
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117
Q

4 factors that influence development of an infarct:

A
  • Nature of vascular supply- single (spleen) or dual (lung, small bowel)
  • Rate of development of occlusion- rapid occlusion more likely to cause infarction
  • Vulnerability of affected tissue to hypoxia- more metabolically active tissue more vulnerable eg. heart
  • Oxygen content of blood- hypoxia increases risk
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118
Q

types of infarct

A

Red (haemorrhagic):

  • Venous occlusion eg. torsion
  • Loose tissues
  • Tissues with a dual circulation eg. lung

White (anaemic)- Arterial occlusions, in solid organs eg. heart, spleen

Septic- Infected infarcts

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119
Q

histology of infarction (stages)

A
  • Ischaemic coagulation necrosis (minutes-days): liquefactive necrosis in the CNS
  • Inflammatory response (hours-7days)
  • Reparative response (1-2 weeks)
  • Scarring (2 weeks-2 months)
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120
Q

pressure of pulmonary and systemic circulations

A

Pulmonary circulation- low pressure circulation

Systemic circulation- high pressure circulation

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121
Q

BP=

A

cardiac output (CO) x peripheral resistance (PR)

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122
Q

Systemic hypertension definition

A
  • Sustained resting BP above certain level
  • 140/90 (depends)
  • Diastolic pressure determine severity
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123
Q

risk factors of primary systemic hypertension

A
  • Idiopathic (unknown cause)
  • Risk factors: genetic susceptibility, high salt intake, chronic stress (excessive sympathetic activity), abnormalities in renin/angiotensin-aldosterone (renin hypertension is v sensitive to ACE inhibitors), diabetes mellitus
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124
Q

Causes of secondary systemic hypertension

A
  • Renal disease: chronic renal failure, polycystic kidneys
    Endocrine causes:
    • Pituitary- ACTH
    • Adrenal cortex- glucocorticoid; mineralocorticoid
    • Adrenal medulla - catecholamines
  • coarctation of the aorta
  • Potentially treatable- test the urine for renal!
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125
Q

pathology of benign and malignant hypertension

A

Benign hypertension- slow changes in vessels and heart with chronic end-organ dysfunction
Malignant hypertension- rapid changes in vessels with acute end-organ dysfunction, BP tends to be higher

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126
Q

end organ effects of hypertension

A

heart: cardiac failure, ischaemic heart disease
kidney: acute renal failure (malignant)
vascular: acceleration of atherosclerosis, Intimal proliferation and hyalinisation (glassy change) of arteries and arterioles

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127
Q

ischaemic heart disease definition and causes

A
  • Blood supply to heart is insufficient for its metabolic demands
    Deficient supply causes:
    • Coronary artery disease (commonest)
    • Reduced coronary artery perfusion- shock, severe aortic valve stenosis (tight)
  • Excessive demand: pressure and volume overload
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128
Q

causes of pressure and volume overload on heart

A

Pressure overload: eg, hypertension, valve disease

Volume overload: eg. valve disease

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129
Q

coronary artery disease

A
  • narrowing or blockage of the coronary arteries
  • Coronary blood flow is normally independent of aortic pressure
  • Initial response to narrowing is autoregulatory compensation
  • > 75% occlusion leads to ischaemia
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130
Q

causes of coronary artery disease

A
  • Atheromatous coronary artery disease (most common):
    • Progressive stenosis
    • Haemorrhage into a plaque
    • Thrombosis
  • Emboli eg. from inflamed aortic valve (endocarditis)
  • Vasculitis- inflammation of coronary arteries
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131
Q

myocardial infarction

A
  • An area of necrosis of heart muscle resulting from reduction (usually sudden) in coronary blood supply
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132
Q

cause of MI

A

rupture of atherosclerotic plaque in coronary artery due to increase in demand in the presence of ischaemia

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133
Q

types of chronic ischaemic heart disease

A
  • Chronic angina- exercise induced chest pain
  • Heart failure- Related to reduced myocardial function
    there is usually widespread coronary artery atheroma and areas of fibrosis often present in the myocardium
134
Q

what can cardiac failure lead to?

A

under perfusion which causes fluid retention and increased blood volume

135
Q

speeds of cardiac failure

A

Acute heart failure- acute onset of symptoms, often with definable cause eg. myocardial infarction
Chronic heart failure- slow onset of symptoms, associated with eg. ischaemic or valvular heart disease
Acute on chronic- chronic failure becomes decompensated by an acute event

136
Q

causes of heart failure

A
  • Pressure overload
  • Volume overload
    Intrinsic cardiac disease:
    • Ischaemic heart disease
    • Primary heart muscle, pericardial & conduction system disease
    • Myocarditis
137
Q

left ventricular failure

A
  • Dominated hypertensive and ischaemic heart failure
  • Causes pulmonary oedema with associated symptoms
  • Leads to pulmonary hypertension and eventually right ventricular failure
  • Combined left and right ventricular failure= congestive cardiac failure
138
Q

Right Ventricular Failure

A
  • Secondary to left ventricular failure

- Related to intrinsic lung disease- cor pulmonale eg. COPD

139
Q

clinical features of forward and backwards failure

A

Forward failure
• Reduced perfusion of tissues
• Tends to be more associated with advanced failure
Backward failure
• Due to increased venous pressures
• Dominated by fluid retention and tissue congestion

140
Q

left and right ventricular failure clinical features

A 
Left Ventricular Failure: 
-	Hypotension
-	Pulmonary oedema
-	Paroxysmal nocturnal dyspnoea
Right ventricular failure:
-	Ankle swelling
-	Hepatic congestion
141
Q

cardiomyocytes

A

heart muscle cells, aligned in sheets that wrap around heart

142
Q

preload definition and causes of increase in preload

A

Preload- volume of blood in the ventricles at the end of diastole, determined by:

  • Blood volume
  • Venous tone
  • Capacity of venous circulation to hold blood
143
Q

afterload definition and causes of increase in afterload

A 
Afterload- resistance the heart must overcome to circulate blood in systole, determined by:
-	Tone in arterial circulation
Increase is caused by:
-	SNS activation
-	Hypertension
144
Q

Coronary artery spasm-

A

spontaneous spasm of smooth muscle cells in coronary artery

145
Q

causes of endothelial dysfunction

A
  • Elevated and modified low density lipoprotein eg. in familial hypercholesterolaemia
  • Oxygen free radicals caused by smoking, hypertension, activated inflammatory cells
  • Infection microorganisms: herpes virus, Chlamydia pneumonia, H. pylori
  • Diabetes, ageing, being male
146
Q

formation of atheromatous plaque

A
  • Development of fatty streaks- foam cells are formed by macrophages taking up increased LDL oxidised by interaction with oxygen free radicals, lipids released from foam cells when they die and accumulate in subendothelial space
  • Fibrous cap- growth factors released by damaged endothelial cells and macrophages cause proliferation of smooth muscle cells which cover plaque on its luminal aspect forming the fibrous cap
  • Stenosis- as the volume of plaque increases, accumulated lipid bulges inwards which reduce the luminal area, point of narrowing of the vessel lumen is called a stenosis
  • Plaque rupture- the fibrous cap separates plaque’s lipid core from the bloodstream but is prone to rupture, this trigger platelet activation & aggregation and thrombus formation
147
Q

statins action in lipid lowering

A

Statins- lower cholesterol and low-density lipoproteins (LDL) eg. simvastatin

  • Inhibit HMG CoA reductase- rate limiting step which reduces formation of LDL in the liver
  • also increase the expression of LDL receptors, so they are cleared faster
  • Additionally: improved endothelial function, inhibition of inflammation, plaque stabilization, inhibition of thrombus formation
  • Side effects: muscle pain, abdominal pain or cramping
148
Q

fibrates action in lipid lowering

A

Fibrates eg. bezafibrate, gemfibrozil, fenofibrate

  • Activate intracellular PPARalpha (peroxisome proliferator receptor alpha)
  • Decrease circulating VLDL and triglyceride but also increase protective HDL and LDL uptake
149
Q

ezetimibe action in lipid lowering

A

Inhibits cholesterol absorption at small intestine by binding to NPC1L1 protein- critical mediator of cholesterol absorption in GI epithelial cells

150
Q

how are Fibrates and Ezetimibe used?

A

with statins or as an alternative to statins

151
Q

angina pectoris

A

intermittent chest pain caused by mismatch between demand of oxygen by the heart and supply of oxygen to the heart

152
Q

causes of O2 supply increase and decrease

A

O2 supply decreased by:

  • Coronary artery disease
  • Anaemia

O2 demand increased by:

  • Exercise
  • Tachycardia
  • Hypertension
153
Q

prophylactics that reduce likelihood of angina attack:

A
  • Targets blood vessels: longer lasting nitrate, KATP channel opener
  • Targets heart: beta adrenoreceptor antagonist, calcium antagonist, ‘funny’ channel blocker
154
Q

Drugs that can be taken acutely during angina attack

A

rest, rapid acting organic nitrate eg. Glyceryl Trinitrate

155
Q

problem with use of glyceryl trinitrate and isorobide dinitrate

A

GT- chronic use leads to tolerance i.e. loss of responsiveness so nitrate free periods are needed
ID- can be prophylactic, nitrate free periods required

156
Q

nicorandil: mechanism and effects

A
  • Causes vasodilation by opening ATP sensitive K+ channel in smooth muscle cells
  • Nitrate moiety- releases NO- in structure therefore addition vasodilator action

Effects:

  • Reduces preload and afterload: O2 demand
  • Dilates coronary arteries and can increase O2 supply in coronary spasm
157
Q

beta blockers

A

Beta Blockers

  • Atenolol, metoprolol, bisoprolol
  • Mechanism: block beta-adrenoreceptors, reduce cardiac rate and output, block RAAS, initial vasoconstriction (ultimately vasodilate)
  • Side effects: wheeze, cold peripheries, lassitude, exercise intolerance, bad dreams, impotence, heart block, diabetes
    indications: AF, angina
158
Q

ivabradine

A

Blocks funny current in sino-atrial node cells, thus reduces the rate of spontaneous depolarisation during action potential generation → reduces heart rate and therefore O2 demand
Less side effects than β-blockers, used as alternative or as adjunct to β blocker therapy

159
Q

Calcium Antagonists

A

Calcium Antagonist eg. nifedipine, dilthiazem

  • Prevents opening of voltage dependant Ca2+ channels → prevents Ca2+ entry into cardiac muscle cells from extracellular space → reduces force of contraction and therefor O2 demand
  • Side effects: headaches, flushing, ankle swelling, tachycardia
160
Q

thrombus formation

A
  • Endothelial cells- produce anti-thrombotic mediators to stop blood clotting but when blood vessel walls are damaged, pro-thrombotic molecules are released
  • Collagen exposure
  • Platelet activation- activated when the subendothelial layer is introduced to blood which then stick to area that is damaged and to each other
  • Coagulation cascade- fibrin binds and stabilises clots and stops bleeding
161
Q

why are antiplatelet drugs taken

A

prophylactically to reduce risk of thrombus

162
Q

platelet activation

A
  • collagen exposure and thrombin= activate platelets
  • Platelets release arachidonic acid from phospholipase A2 and it is a precursor for prostaglandin molecules.
  • Cyclic endoperoxidase is formed from arachidonic acid by the enzyme cyclooxygenase.
  • In platelets the main prostaglandin that formed is TxA2 which activates receptors on the platelets which increases the availability of calcium- enables function of platelets.
163
Q

what do activated platelets do?

A

change shape, release contents of granules and express glycoprotein IIb/IIa receptors for attachment of fibrin from coagulation cascade to stabilise thrombus

164
Q

cyclooxygenase inhibitor actions and side effect

A

Cyclooxygenase inhibitor eg. aspirin
Irreversible inhibition of COX, prevents formation of TxA2 & platelet activation, works because platelets have no nucleus and cannot proliferate
Side effect: stomach pain

165
Q

P2Y12 inhibitor action

A

P2Y12 inhibitor e.g. clopidogrel, ticagrelor

Blocks effects of ADP and prevents platelet activation

166
Q

coagulation cascade

A

When blood vessels are damaged, series of proteases activate the coagulation cascade. Factor X activates Xa which then activates prothrombin to become thrombin which activates fibrinogen to become fibrin- stabilises the clot.

167
Q

what does heparin agonise?

A

anti-thrombin III to promote its action

168
Q

warfarin targets

A

Vitamin K pathway

- Reduction of Vitamin K results in the carboxylation of certain factors: II, VII, IX, X

169
Q

warfarin cons

A
  • Narrow optimal range, high risk of bleeding
  • Broken down in liver, enzyme induced by other drugs, environmental influences
  • Blood levels must be checked regularly
170
Q

warfarin clinical indications

A

atrial fibrillation, presence of artificial heart valve, DVT, pulmonary embolism and occasionally after myocardial infarction

171
Q

what often leads to heart failure?

A

MI

172
Q

body’s pro and anti fibrinolytic mechanisms

A

pro- (tissue plasminogen activator)

anti- (PAI-1 antiplasmin)

173
Q

examples of inotropic agents

A
  • Digoxin

- Dobutamine (ß1 adrenoreceptor agonist iv for rapid response), increases heart rate and contractility

174
Q

actions of digoxin and digitalis

A

cardiac glycosides,
mechanism: blocks Na/K ATPase, slows conduction through the AV node, increased force of cardiac contraction
positive inotrope therefore increases kidney perfusion and fluid loss]
- Side effects: anorexia, nausea, vomiting, AV block, renal failure

175
Q

drugs that affect RAAS in heart failure

A
  • Renin inhibitor eg. aliskiren
  • ACE inhibitor eg. enalaspril, linsopril
  • angiotensin receptor antagonists eg. losartan, valsartan
176
Q

function of loop diuretics

A

Loop diuretics eg. frusemide, bumetanide

- Impair Na+/K+/Cl- readsorption in the ascending loop of Henle

177
Q

Mineralocortoid receptor antagonists function

A

Mineralocortoid receptor antagonists eg. spironolactone, eplerenone
- Block effects of aldosterone on NA/K readsorption

178
Q

hydralazine mechanism

A
  • Dilator that targets arteries > veins and reduces afterload
179
Q

when are nitrates and hydralazine used

A

to treat acute heart failure or in patients with chronic heart failure who fail to respond to other drugs.

180
Q

what does the progression of heart failure do to ventricles?

A

ventricle walls become stiffer and thicker

181
Q

fibrosis

A

laying down of collagen, connective tissue replaces normal tissue

182
Q

Important lipids in human physiology:

A
  • Steroids; cholesterol, steroid hormones eg. testosterone
  • Fat soluble vitamins: A, D, E, K
  • Phospholipids
  • Sphingolipids
  • Triglycerides
183
Q

components of lipoproteins

A
  • Cholesterol can be free or esterified
  • Phospholipids
  • Triglycerides
184
Q

solubility of lipids

A

poorly soluble in water but miscible in organic solvents

185
Q

lipoproteins main types

A
  • Chylomicrons- mostly triglycerides, biggest
  • Very Low Density Lipoprotein (VLDL)- big, predominantly triglycerides
  • Intermediate Density Lipoprotein (IDL)- very short lived
  • Low Density Lipoprotein (LDL)- cholesterol-rich, long-lived
  • High Density Lipoprotein (HDL)- small, cholesterol rich, long lived
186
Q

where are lipoproteins created within?

A
  • Small intestine (dietary lipids)
  • Liver (endogenous lipids)
  • These travel to peripheral tissues and back to the above tissue for storage by reverse cholesterol transport
187
Q

exogenous lipid pathway

A

The gut secretes chylomicrons into lymphatic system and then bloodstream. Through bloodstream, they are deposited into main sites of muscle and adipose tissue. They both store fat and triglycerides, muscle can metabolise non esterified fatty acids (NEFA)- produced by breakdown of triglyceride into glycerol and fatty acid. Lipoprotein lipase acts on chylomicrons as it travels and degrades it. Chylomicron remnants are taken up by the liver.

188
Q

what does blood in a test tube look like if chylomicrons are not cleared properly?

A

blood in test tube would separate into an opaque serum of chylomicrons and blood, this is why fasting is important before LDL samples are taken

189
Q

Endogenous Lipid Pathways

A

VLDL from liver travels through bloodstream but can be secreted in fasting stage. It progressively gets degraded by lipoprotein lipase as it travels. It turns into an intermediate density lipoprotein, it either gets taken up by the liver or at the liver it can be broken down by the enzyme, hepatic lipoprotein lipase so IDL become LDL.

190
Q

LDL function

A

transports cholesterol to peripheral tissue

191
Q

reverse cholesterol transport

A

HDL is made in both liver and gut. Free cholesterol in peripheral tissue can be secreted and packaged by LCAT enzyme and included in the payload of HDL particle. HDL travels around taking up cholesterol and then returns to the liver where it is taken up. The cholesterol is stored and secreted into the gut or repackaged into a lipoprotein to be secreted

192
Q

lipids and CV disease

A

Raised HDL-cholesterol: decreased rates of CV disease.

Raised LDL-C: increased rates of CV disease.

193
Q

apolipoproteins

A

proteins that bind lipids to form lipoproteins. They transport lipids in blood, cerebrospinal fluid and lymph

194
Q

what apolipoprotein binds chylomicrons and VLDL?

A

ApoB48

195
Q

what apolipoprotein binds IDL and LDL?

A

ApoB100

196
Q

what apolipoprotein binds HDL

A

ApoA1

197
Q

lipoproteins function

A
  • Transport cholesterol and triglycerides around the body via the circulation
198
Q

triglycerides delivery

A
  • chylomicrons, created in the gut, deliver triglycerides to muscle & adipose tissue (where converted to NEFA)
  • VLDLs, synthesized in liver, also deliver triglycerides to muscle & adipose tissue (again converted to NEFA)
199
Q

cholesterol delivery

A
  • Liver is the master organ: synthesis, secretion, uptake, excretion
  • Delivered to peripheral tissues via LDL
  • Uptake from circulation via remnants, IDL, LDL, HDL
  • Returned to liver (from peripheral tissues) via HDL
200
Q

how are oxygen free radicals formed?

A
  • glycation reactions (diabetes)
  • toxins from cigarette smoke
  • macrophages
201
Q

what can high conc of LDL lead to

A

formation of fatty streaks: LDL + monocytes + O-free radicals

202
Q

familial hypercholestrolaemia

A
  • Autosomal dominant
  • Mutation in LDL receptor (or ApoB, PCSK9)
  • High LDL-C levels (typically >4.9 mmol/L)
  • Untreated leads to premature CHD onset
  • Statin treatment shown to reduce CVD risk
203
Q

Routine laboratory measurements of lipids:

A
  • total cholesterol
  • HDL cholesterol (HDL-C)
  • triglycerides
  • LDL is calculated by friedelwald equation (not measured)
204
Q

MI acute treatment

A
  • reperfusion via primary PCI

- drug-eluting stents (anti-proliferative agent so prevents re-occlusion)

205
Q

primary prevention of CVD

A
  • diet- reduce saturated fats, simple carbs, salt
  • aerobic exercise
  • aim for BMI 20-25
  • reduce alcohol
  • quit smoking
206
Q

drugs for secondary prevention of CVD

A
  • ACE-inhibitor, Beta-blocker – reduce post-MI mortality
  • Aspirin + Clopidogrel – reduce CVD recurrence & mortality
  • Statins – reduce CVD recurrence & mortality
207
Q

effect of statins and ezetimibe on LDL-C

A
  • Reduce LDL-C

- Lower risk of coronary heart disease

208
Q

PCKS9 inhibitors

A
  • monoclonal antibodies that are delivered by fortnights s/c injection
  • Capable of ~60% reduction of LDL-C (as adjunct to statin)
209
Q

regulation of the coagulation cascade

A
  • TF-2a complex/f10a inhibited by TFPI, tissue factor pathway inhibitor of extrinsic
  • Thrombin and f10a activity inhibited by Antithrombin pathway
  • Protein C pathway inhibits activation of f5a and f8a
210
Q

risk factors of venous thromboembolism

A
  • Age
  • Obesity
  • Varicose veins
  • Previous VTE
  • Family history of VTE
  • opophilia- high risk would be anti-thrombin deficiency
  • Cancer
211
Q

types of VTE

A
  • DVT
  • Pulmonary embolus
  • Cerebral, mesenteric, axillary, splanchnic, splenic
212
Q

clinical features of Lower Limb DVT

A
  • Pain, swelling, increased temp of limp, dilation of superficial veins
  • Usually unilateral
  • May be bilateral if thrombosis sited in vena cava
213
Q

well’s score

A
  • Stratify patients into low, intermediate and high probability categories for VTE
214
Q

testing for DVT

A
  • Most useful objective objective tests are compression USS and D-dimer
  • Venous ultrasonography
  • Non- compressibility of the common femoral vein or popliteal vein are diagnostic of DVT
  • Contrast venography
215
Q

Clinical features of PE

A
  • Collapse, faintness, crushing central chest pain
  • Pleuritic chest pain
  • Difficulty breathing
  • Haemoptysis
  • Exertional dyspnoea
216
Q

diagnosis of PE

A
  • CXR- to exclude any other pathology
  • ECG
  • Arterial blood gases
  • Echocardiogram- look for right ventricular strain
217
Q

types of anticoagulant therapy

A
  1. Rapid initial anticoagulation
    - Parenteral anticoagulant: heparin, low molecular weight heparin, fondaparinux, OR
    - Direct oral anticoagulant
  2. Extended Therapy
    - Orally active anticoagulant: Vitamin K antagonist (warfarin)
    - Or direct anti oral coagulant
218
Q

direct oral anticoagulants

A
  • Dabigatran, Rivaroxaban, Edoxaban & Apixaban
  • Enables rapid initial anticoagulation orally
  • Continue a maintenance dose for 6 months or longer for secondary prevention of VTE
  • Apixaban and Rivaroxaban do not need any overlap with heparin – big advantage in outpatient setting
219
Q

thrombophilla signs

A
  • Venous thrombosis <45 yrs
  • Recurrent venous thrombosis
  • Family history of unprovoked thrombosis
  • Combined arterial and venous thrombosis
220
Q

types of heparins

A

Unfractionated- Sulphated glycosaminoglycan, binds to plasma proteins, heterogenous group of molecules with MW from 3000 to 30,000D

LMW- Binds to unique pentasaccharide on antithrombin and potentiates its inhibitory action towards factor Xa and thrombin, reduced capacity to inhibit thrombin compared with UFH, predictable anti-coagulant response and dose-dependent renal clearance

221
Q

when is UFH used?

A
  • Used when there is a high risk of bleeding
  • Reverse by d/c infusion and also protamine
  • Monitoring required
  • Risk of osteoporosis, heparin-induced thrombocytopenia (HIT)
222
Q

LMWH properties

A
  • Irreversible
  • Nearly 100% bioavailability means reliant dose dependant coagulant effect
  • Generally no monitoring required
  • Reduced risk of osteoporosis and HIT
223
Q

direct oral anticoagulant indications

A
  • Treatment of DVT and PE

- Prevention of cardioembolic events in patients with atrial fibrillation

224
Q

prevention methods of venous thromboembolism

A
  • Mechanical: mechanical foot pumps, graduate compression stockings
  • Pharmacological: LMWH, UFH, fondaparinux, dabigatran, rivaroxaban, warfarin
225
Q

benefits of DOACs over warfarin

A
  • More predictable anticoagulant profile
  • Fewer drug and food interactions
  • Wider therapeutic interactions & window
  • Oral administration
  • No need for monitoring
226
Q

what stabilises a platelet thrombus?

A

conversion of fibrinogen to fibrin by thrombin and polymerisation of fibrin

227
Q

Thrombocytopenia caused by

A 
Bone marrow failure
	Peripheral consumption (eg. immune TP, DIC, drug-induced)
228
Q

clinical features of Thrombocytopenia

A
  • All give rise to a prolonged bleeding time

- Reduced number of platelets

229
Q

reasons for abnormal Platelet Function:

A
  • Most commonly drugs such as aspirin, clopidogel

- Renal failure: uraemia

230
Q

reasons for Abnormal Vessel wall:

A
  • Scurvy
  • Ehlers Danlos syndrome
  • Henoch Schӧnlein purpura
  • Hereditary Haemorrhagic Telangiectasia
231
Q

disease that causes abnormal Interaction between Platelets and Vessel Wall

A

Von Willebrand disease

232
Q

drugs that inhibit platelet function

A
  • Aspirin and COX inhibitors
  • Reversible COX inhibitors
  • Dipyridamole- inhibits phosphodiesterase
  • Thienopyridines- inhibit ADP- mediated activation eg. clopidogrel
233
Q

Prothrombin Time

A
  • Measured in secs

- Reflects extrinsic and common pathways

234
Q

Activated Partial Thromboplastin Time

A
  • Measured in secs

- Reflects the intrinsic and common pathways

235
Q

Measurement of fibrinogen (g/L)

A
  • Reflects the functional activity of the fibrinogen protein
236
Q

haemophilia A

A
  • X linked recessive disorder (typically expressed in males and carried in females)
  • Most cases due to sporadic mutation
  • Deficiency of fVIII (or dysfunction)
  • Severity of haemophilia same in different generations
  • Normal fVIII level ranges from 50-150% but mild form of haemophilia is below 30%
237
Q

Traditional Management of Haemophilia

A
  • Supportive measures: ice, immobilisation, rest
  • Replacement of missing clotting protein:
    • Coagulation factor concentrates
    • Desmopressin used to increase factor VIII levels in mild/moderate haemophilia A
    • Novel therapies- monoclonal antibodies, knock-out AT
  • Antifibrinolytic Agents: tranexamic acid
238
Q

Congenital Vs Acquired Haemophilia

A

Congenital: hemarthroses, muscle bleeds, soft tissue bleeds
Acquired: large haematomas, gross haematuria, cerebral haemorrhages, compartment syndromes

239
Q

Roles of Von Willebrand Factor

A
  • Promote platelet adhesion to subendothelium at high shear rates
  • Carrier molecule for FVIII
  • Most common heritable bleeding disorder- mainly autosomal dominant
  • Variable reduction in factor VIII levels- mucocutaneous bleeding including menorrhagia, post-operative and post partum bleeding
240
Q

Management of Von Willebrand Disease

A
  • Antifibrinolytics- tranexamic acid
  • DDAVP (for type 1 vWD)
  • Factor concentrates containing vWD
  • Contraceptive pill for menorrhagia
241
Q

acquired coagulation disorders

A
  • Underproduction of coagulation factors- liver failure or Vit K deficiency
  • Immune: acquired haemophilia, acquired VW syndrome
  • Consumption of coagulation factors: DIC
242
Q

liver disease and coagulation disorder

A
  • Reduced hepatic synthesis of clotting factors
  • Thrombocytopenia secondary to hypersplenism
  • Reduced vitamin K absorption due to cholestatic jaundice causing deficiencies of factors II, VII, IX & X
  • Treat with plasma products and platelets to cover procedure and Vit K
243
Q

DIC

A
  • Acquired syndrome of systemic intravascular activation of coagulation
  • Widespread deposition of fibrin in circulation
  • Tissue ischaemia and multi-organ failure
  • Consumption of platelets and coagulation factors to generate thrombin may induce severe bleeding
  • To maintain vascular patency, plasmin generated in excess leads to fibrinogenolysis
244
Q

causes of DIC

A
  • Sepsis
  • Tumour
  • Pancreatitis
  • Transfusion of ABO incompatible cells
245
Q

DIC coagulation features

A
  • Prolonged prothrombin time
  • Prolonger activated partial thromboplastin time
  • Low fibrinogen
    (markers of consumption of coagulation factors)
    • Raised D dimers (marker of increased fibrinolysis)
246
Q

Ventricular contraction and relaxation

A
  • Ventricular contraction- contraction of ventricles pushes blood into elastic arteries causing them to stretch
  • Ventricular relaxation- elastic recoil in the arteries maintains driving pressure during ventricular diastole
247
Q

stiff large arteries and BP

A
  • Cause a higher systolic BP leading to higher stroke and MI risk
  • Cause a lower diastole BP reducing coronary artery filling
248
Q

genetics of BP

A
  • 30-50% genetic heritability
  • Genes are mostly found in the kidney
  • Affect movement of electrolytes in and out of kidney so salt handling in the kidney is critical for high blood pressure
249
Q

prioritise BP treatment for

A
  • Older people (50+)
  • Diabetics
  • People with other CVS risk factors (lipids, smoking ect.)
250
Q

stages of high BP

A

Stage 1: Clinic BP >140/90
Stage 2: Clinic BP >160/90
Stage 3: Clinic BP >180/110

251
Q

calcium antagonists reduce symptoms in

A

angina and isolated systolic hypertension

252
Q
  • Diuretics (thiazide-like) have benefits in
A

heart failure

253
Q

ACE inhibitors

A
  • Enalapril, lisinopril, ramipril
  • Mechanism: inhibit ACE, block RAAS, increase bradykinin, dilate arteries (and veins)
  • Side Effects: cough, renal dysfunction, dizziness, rash
254
Q

thiazide drugs mechanism

A

mechanism: inhibit Na+/Cl- symport, distal tubular natriuresis, dilates arteries and veins

255
Q

drug related secondary causes of BP

A
  • Oestrogen oral contraceptives
  • Liquorice/ carbenoxolone/ steroids
  • Non-steroidal anti-inflammatory (NSIADs)
  • Sympathomimetics including cocaine
  • Alcohol
256
Q

what does he foetal ductus venosus become in adults?

A

ligamentum venosum

257
Q

combo of which 2 drugs can cause asystolic cardiac arrest?

A

beta-blockers and calcium channel blockers

258
Q

what is spontaneous activation of the sinus node caused by?

A

leak of calcium into the sinus node

259
Q

effect of sympathetic nerves on heart

A

Sympathetic nerves release adrenaline onto the surface of the heart which can increase the depolarisations and the contractility of the heart.

260
Q

effect of parasympathetic nerves on heart

A

Parasympathetic nerves come into the heart from the brain stem and the vagus nerves innervate the heart as well as other structures in the body. When these nerves are active, they slow the heart down.

261
Q

parasympathetic and sympathetic systems at rest and exertion

A

In the resting state, the parasympathetic system is active and the sympathetic isn’t.
While exercising, the parasympathetic system becomes inactive and that causes an increase in heart rate where the sympathetic system becomes active.

262
Q

impulse propagation in the heart

A

The sinus node activates and causes a ripple effect through the atria.
The AV valves which are between the atria and ventricles (mitral valve- left, tricuspid valve- right) are made of fibrous tissue that doesn’t conduct electrical signals so there is no way for electrical impulse to pass from atria to ventricles other than the AV node.
The AV node conducts slowly compared with the rest of the heart which introduces a 0.15s time delay between atrial contraction and ventricular contraction, this gives time for the atria to contract and ventricles to fill with blood before contracting and deliver blood to body/lungs.
Once the impulse reaches the ventricles, rapid conduction is achieved through the bundle of His, the right/left bundle branches and the Purkinje fibres.
This allows the ventricles to contract simultaneously giving a good cardiac output.

263
Q

why is the PR interval small?

A

because the atrial muscle doesn’t have a lot of muscle mass.

264
Q

what does the QRS complex reflect

A

ventricular contraction

  • Large QRS complexes- large ventricular mass like in high BP
  • Wide QRS complexes- taking longer than normal for ventricular activation, could be problem with smaller fibres (eg. His, Purkinje, bundles)
265
Q

what does the T wave reflect

A

ventricular repolarisation

266
Q

sinus arrhythmia

A
  • Sinus node fires at a variable rate
  • Speeds up during inspiration and slows down during expiration
  • Effect caused by variations in vagus nerve activity
267
Q

sinus tachycardia and causes

A
  • Sinus node fires >100 per minute
  • Physiological causes: anxiety, exercise
  • Pathological causes: fever, anaemia, hyperthyroidism, heart failure
268
Q

sinoatrial disease

A
  • Degenerative disease where healthy muscle around sinus node is replaced by scar tissue, fibrous tissue and fatty tissue
  • Mixture of sinus tachycardia, bradycardia and atrial ‘ectopic’ beats, atrial fibrillation
269
Q

treatment of sinoatrial disease

A
  • Permanent pacemaker to prevent slow rhythms

- Antiarrhythmic drugs (eg. digoxin, amiodarone) to prevent rapid rhythms

270
Q

Sinus Bradycardia and causes

A
  • Sinus node fires <60 beats per minute
  • Physiological causes: sleep, athletes
  • Pathological causes: hypothyroidism, hypothermia, sinus node disease raised intracranial pressure
271
Q

AV nodal blocks- types and features

A
  • Long PR interval- issue with AV nodal conduction
  • First degree AV nodal block- delay to conduction in AV node
  • Second degree AV nodal block: Wenckebach conduction- PR interval gradually increases, leads to pauses in ventricular rhythm,
  • Sometimes QRS complex can be dropped which indicates problems with bundle of His
272
Q

causes of AV nodal block

A 
•	Sino-atrial disease
•	coronary heart disease
•	aortic valve disease
•	drugs 
– beta-blockers
– digoxin
– calcium channel blockers
273
Q

treatment of AV nodal block

A
  • remove any triggering cause eg. drugs
  • atropine or isoprenaline (acute treatment)
  • permanent pacemaker
274
Q

atrial fibrillation and flutter

A
  • irregularly irregular rhythm
  • Apical radial deficit- every time the aortic valve closes, sometime a pulse won’t be felt (too little blood pushed out)
  • atria contract at rapid and uncoordinated manner
  • some people who are prone to atrial fibrillation are also prone to atrial flutter- regular rapid activation of atria
275
Q

Causes of Atrial Flutter/ Fibrillation:

A
  • Sino atrial disease
  • Coronary heart disease
  • Valve disease (esp. mitral valve)
  • Hypertension
  • Cardiomyopathy
276
Q

treatment of atrial fibrillation and flutter

A
  • Drug to block AV node and therefore limit heart rate eg. digoxin or beta blocker
  • Electrical cardioversion
  • Catheter ablation- wires into heart to target tissue that cause atrial fibrillation
277
Q

ventricular fibrillation

A
  • Heart rate over 150 beats
  • Broad complex (wide QRS complex) tachycarida- originates from the ventricles
  • In most cases, can be life threatening
278
Q

treatment of ventricular fibrillation

A
  • Defibrillation
  • Anti-arrhythmic drugs
  • Remove any triggering cause
  • Implantable defibrillator for some patients
279
Q

anastomoses

A

connections between diverging blood vessels

280
Q

what can compensate for occlusion of the main system in some circumstances?

A

Collateral circulation

281
Q 
dilated artery= 
narrowed artery= 
split artery=
blocked artery= 
inflamed artery= 
oversensitive artery=
A 
o	Dilated= aneurysm
o	Narrowed= stenosis
o	Blocked= occluded
•	Split= dissection
•	Over sensitive= vasospasm
•	Inflamed= vasculitis
282
Q

aneurysm

A
  • Defined by arteries being 1.5 times the normal diameter
  • Degenerative aneurysms are the most common- occur when the connective tissue and muscular layer of the aorta weakens and gets thinner, which increases the chances that it will rupture or dissect, happens most often in descending thoracic aorta or abdominal aorta
283
Q

stenosis

A
  • Atherosclerosis, also leads to occlusion after plaque rupture
    symptoms:
  • Claudication- pain on walking a fixed distance which is worse uphill, eases rapidly when you stop, angina of the leg
  • Short distance claudication
  • Nocturnal pain/ rest pain
284
Q

treatment of claudication

A
  • Quit smoking
  • Aspirin
  • Atorvastin
285
Q

acute symptoms of occlusion (6Ps)

A
  • Pain (sudden onset)
  • Palor- extreme or unnatural paleness
  • Perishingly cold
  • Parasthesia- abnormal sensations of skin
  • Pulselessness
  • Paralysis
286
Q

chronic symptoms of occlusion

A
  • Short distance claudication
  • Nocturnal pain
  • Pain at rest
  • Numbness
  • Tissue necrosis
287
Q

vasospasm

A
  • Overactive vasoconstriction
  • Capillary beds shut down
  • Triggers- cold, stress
  • Can have underlying connective tissue disease
288
Q

vasculitis

A
  • Large vessel: Takayasu’s disease, ‘the pulseless disease’
  • Medium vessel: Giant cell arthritis/ polymyalgia
  • Small vessel: lots of polyangiitis conditions usually involving kidney
289
Q

treatment of vasculitis

A

steroids or other immunosupressants

290
Q

broken artery causes

A

trauma, self-inflicted, latrogenic (due to physician or therapy)

291
Q

diabetic foot

A
  • Neuropathic
  • Ischaemic
  • Infected
  • Calcified vessels
  • Small vessel arterial disease
  • Can’t see their own foot (retinopathy)
292
Q

Charcot foot (end stage diabetic foot changes)

A

o Neuropathic
o Warm (>2C than normal)
o Multiple fracture
o “Rocker bottom” sole

293
Q

Valve Failure in superficial and deep veins

A
  • Superficial veins= varicose veins

- Deep veins= venous hypertension

294
Q

venous hypertension symptoms

A
  • Hemosiderin staining
  • Swollen legs
  • Itchy, fragile legs
  • Gaiter distribution (shinpad)
  • Risk of ulceration
295
Q

treatment for venous hypertension

A
  • Emollient to stop skin cracks
  • Compression: bandages, wraps, stockings
  • Elevate and mobilise
296
Q

Phlegmasia and Venous Gangrene

A
  • Phlegmasia= rare form that results from extensive thrombotic occlusion
  • Often with underlying cancer
  • Treatment: thrombolysis
297
Q

Porto-systemic venous system

A
  • Mesenteric or ‘portal venous’ drainage is via the liver before the heart
  • Systemic circulation is returned to the heart directly
  • The two circulation systems combine at a number of points
298
Q

portal hypertension development and body’s recovery

A

In liver disease the portal system fails to drain and portal hypertension develops. Blood is therefore diverted into the systemic venous system → Porto-systemic venous anastomoses

299
Q

where does the lymphatic system drain?

A

thoracic duct and ultimately to left subclavian vein

300
Q

lymphoedma cause

A

Under normal circumstances the lymphatic system collects interstitial fluid and ultimately returns to the circulation. If the lymphatic channels are blocked interstitial fluid accumulates which leads to lymphoedema.

301
Q

Lymphoedema Treatment

A
  • Compression
  • Skin care
  • Exercise
  • Manual lymphatic drainage: specialised massage technique
  • Rarely surgery to debulk, liposuction or connecting lymph channel to veins
302
Q

causes of reduced oncotic pressure

A
  • Liver failure
  • Renal disease- low protein or too much water
  • Malnutrition- kwashiorkor (severe protein malnutrition- oedema)
    Low protein (albumin) states lead to limb swelling and oedema.
303
Q

starling forces

A

the forces created by the hydrostatic and oncotic pressure due to blood and extracellular fluid

  • Hydrostatic= out of the capillary. Greater at the arteriole side of the capillary
  • Oncotic= into the capillary. Greater at the venule side of the capillary
304
Q

movement of water due to interstitial pressure (each have an effect on the tendency for water to move into or out of the capillary)

A
  • The hydrostatic pressure of blood forces water out of the capillary
  • The hydrostatic pressure of interstitial fluid tends to draw water out of the capillary
  • The oncotic pressure of plasma draws fluid into the capillaries
  • The oncotic pressure of interstitial fluid draws water out of capillaries
305
Q

filtration and reabsorption in capillary fluid exchange

A
  • At the arteriole end, high blood pressure is greater than osmotic pressure and fluid is forced out resulting in high solute concentration in the blood (FILTRATION)
  • At the venule end, blood pressure is low as blood has been diverted to many arterioles and osmotic pressure (
306
Q

in what way can the Starling equilibrium be disturbed to allow water accumulation in the interstitial space?

A

net capillary filtration exceeds capacity for lymphatic drainage

307
Q

factors that increase net filtration

A
  • Increased hydrostatic pressure- favours filtration over absorption
  • Decreased oncotic pressure- reabsorption is reduced and net filtration is increased
  • Increased capillary permeability- results in loss of protein from the plasma into the interstitial space which increases oncotic pressure and promotes net filtration
308
Q

arterial blood pressure=

A

CO x SVR (Systemic Vascular Resistance)
SVR- majority of vascular resistance is provided by arterioles, change in tone of smooth muscle results in blood flow to be diverted from one vascular bed to another

309
Q

causes of increase in myocardial contractility

A

Myocardial Contractility

Increased by: noradrenaline, adrenaline, beta-1 adrenoreceptors

310
Q

cause of cardiac arrhythmia

A

physiological:
1. Increase in automaticity: cells that are normally quiescent starting to depolarise spontaneously
2. Re-entry: re-entry of the wave of depolarisation back to higher levels allowing rapid circus movement (rare)
Clinical: drugs, electrolyte imbalance, coronary heart disease leading to ischaemia within the conduction system and myocardium, congenital

311
Q

what is blood vessel smooth muscle directly innervated by?

A

post-ganglionic sympathetic nerve endings which release noradrenaline to act as an antagonist at alpha-1 adrenoreceptors and cause vasoconstriction.
Some muscles cause vasodilation by acting at beta-2 adrenoreceptors.

312
Q

Smooth muscle tone is under influence of

A

locally secreted factors like endothelin (vasoconstrictor) and NO (relaxer).

313
Q

arterial baroreceptors are

A

Specialised mechanoreceptors that respond to stretch in the adventitial layer or the artery by producing action potentials

314
Q

sites of arterial baroreceptors

A
  • carotid sinus- signals travel in glossopharyngeal nerve, can sense ABP seen by cerebral circulation
  • aortic arch- signals travel in vagus nerve, can sense ABP seen by heart and other major organs
315
Q

what can BP be increased/decreased by?

A

increased by the vasoconstrictor phenylephrine.

reduced by the vasodilator glyceryl trinitrate.

316
Q

where do baroreceptor signals travel to

A

vasomotor centre in the medulla oblongata that is responsible for homeostatic reflexes
Many efferent responses are coordinated by the autonomic nervous system.

317
Q

baroreflexes

A

provide second to second control of blood pressure
Baroreflexes can be tested using tilt table testing where rapid movement from the lying position require prompt increases in heart rate to maintain blood pressure

318
Q

baroreflexes in young vs old

A

extremely sensitive in younger individuals allowing them to withstand changes in posture without threatening blood pressure and immediate cerebral perfusion
elderly have less sensitive baroreflexes: less able to increase heart rate to maintain blood pressure, less able to tolerate sudden changes to systolic blood pressure
Hypertension means that baroreflexes must reset to allow base blood pressure at a higher point.

319
Q

supreventrivcular tachycardia presentation

A
  • Palpitations
  • Rapid regular pulse (160-180/min)
  • Often in young patients
    Problem: rapid re-entry through the AV node
320
Q

supreventrivcular tachycardia management and prevention

A
  • Vagal stimulation manoeuvres- carotid massage, Valsalva, eyeball pressure, diving reflex
  • Immediate treatment: adenosine, verapamil, synchronised DC cardioversion (if drugs fail and rapid control required)
  • Prevention: verapamil orally, surgical ablasion (normalises heart rate)
321
Q

adenosine

A
  • Natural endogenous purine
  • Mechanism: a1 receptors in the AV node (K+ channels), hyperpolaristion of conduction tissue, transient blockage of conduction through the AV node, temporarily abolishes re-entry through the AV node
  • Indications: supraventricular tachycardia
  • Side effects: chest pain dyspnoea, dizziness, nausea
322
Q

verapamil

A
  • Calcium channel blocker
  • Mechanism: blocks voltage sensitive L type calcium channels, lower conduction through the SA and AV nodes, lower force of contraction of heart, vasodilation
  • Indications: SVT, AF, angina, hypertension
323
Q

ventricular tachycardia

A
  • Series of 3 or more ventricular ectopic beats
  • Increase in automaticity of ventricular tissue
  • Serious- often causes significant haemodynamic disturbance with hypotension, heart failure
  • May deteriorate to cardiac arrest
  • Cause: myocardial ischaemia (reperfusion)
324
Q

amiodarone

A
  • Class III anti-arrhythmic drug
  • Mechanism: prolongs cardiac action potential, blocks potassium channels
  • Indications: highly effective multipurpose antiarrhythmic, atrial and ventricular arrhythmias
  • Side effects: toxic, reversible corneal microdeposits, photosensitivity, pulmonary fibrosis, hepatitis, thyroid dysfunction
325
Q

treatment of complete heart block

A

pacemaker, atropine

326
Q

streptokinase

A

thrombolytic medication, which breaks down clots. It may be used in myocardial infarction, pulmonary embolism or ischaemic/thromboembolic stroke.

327
Q

tetralogy of fallot

A

ventricular septal defect , pulmonary valve stenosis, a misplaced aorta and a thickened right ventricular wall

328
Q

which factors relax blood vessels by generating NO?

A

Sheer stress/blood flow, acetylcholine, bradykinin and Substance P all relax blood vessels by generating NO.

329
Q

what kinds of plaques are at greatest risk of rupture?

A

Plaques which have a thin fibrous cap, large lipid pool and large inflammatory cell infiltrate are at greatest risk of rupture.

330
Q

Treatment for varicose veins

A

endothermic ablation, surgical removal, foam sclerotherapy, adhesive occlusion, compression

331
Q

cardiac rupture sequence of events after MI

A

weakening of wall by necrosis -> cardiac rupture -> haemopericardium -> cardiac tamponade -> cardiac arrest

332
Q

pericarditis after MI

A

causes sharp chest pain and normally occurs within 2-4 days

Y1S2- Cardio, Resp, Loco (3 decks)

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