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phase 2 cardiovascular and respiratory block > week 1 > Flashcards

week 1 Flashcards

1
Q

locations of heart valves

A

tricuspid - RA-RV
mitral/bicuspid - LA-LV
pulmonary - RV-PA
aortic - LV-aorta

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2
Q

cardiac cycle

A

atrial systole
atrial diastole
ventricular systole
ventricular diastole

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3
Q

function of atrial systole

A

atrial contraction forces small amount of additional blood into relaxed ventricles

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4
Q

ventricular systole

A

first phase - ventricular contraction pushes AV valves closed but not enough pressure to open semilunar valves
second phase - ventricular pressure rises and exceeds pressure in arteries - S valves open and blood is ejected

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5
Q

ventricular diastole

A

early - as ventricles relax, pressure here drops and blood flows back against s valves, forcing them shut - blood flows into relaxed atria
late - all chambers relaxed, ventricles fill passively

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6
Q

positive inotropy

A

greater contraction

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7
Q

cardiac output equation

A

CO = SV x HR

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8
Q

BP equation

A

BP = CO x PVR

PVR is peripheral vascular resistance

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9
Q

how is the membrane potential in cardiac cells maintained

A

Na+ and Ca2+ current inwards is depolarising - high conc outside cell
K+ current outwards repolarises - high conc inside

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10
Q

action potential phases

A

0 - opening of voltage gated Na+ channels allowing Na+ inwards
1 - rapid membrane voltage dependent inactivation of I(Na) - activation of outward K+
2 (plateau phase) - balance of inward Ca2+ and outward K+
3 (repolarisation) - inward currents inactivated and outward K+ predominant
4 - resting

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11
Q

excitation-contraction coupling

A

1 - membrane depolarisation
2 - this activates L type Ca channel
3 - Ca induced Ca release - RyR sits next to L type Ca channel in cell and sense local calcium - Ryr then opens and pours Ca from SR
4 - Ca binds to myofilaments initiating contraction
5 - relaxation - calcium released from SR goes back in and Ca from outside cell is pumped out of cell
6 - return to resting Ca levels

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12
Q

where do coronary arteries arise

A

from base of aorta

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13
Q

coronary arteries

A

left coronary artery splits to left circumflex and left anterior descending
left marginal artery from LCA
right coronary artery splits into posterior descending and right marginal

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14
Q

how does blood get into coronary arteries

A

during diastole

blood travels back in aorta and down coronary arteries

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15
Q

where to auscultate valves

A

aortic valve at 2nd-3rd right interspace
pulmonary valve - 2nd-3rd left interspace
tricuspid - left sternal border
mitral - apex

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16
Q

what is phenylephrine

A

a1 adrenoreceptor agonist
causes powerful vasoconstriction
adrenaline and noradrenaline will stimulate normally

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17
Q

what are the holes in the internal lamina for

A

endothelial cells can communicate with SMCs

remodelling reduces connection

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18
Q

effect of pressure on vascular structure

A

vessel widens
wall gets thinner
vessel gets longer - SMCs are arranged in helical structure
systole - blood

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19
Q

what is pulse wave velocity

A

velocity at which the blood pressure pulse propagates through the circulatory system
more springy, stretchy arteries will dampen wave making PWV lower
high PWV may be vascular stiffening

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20
Q

main change to vessels in hypertension

A

hypertension results in vascular remodelling

remodelling characterised by increased media to lumen ratio - media thickens - lumen narrows

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21
Q

how does blood vessel radius affect flow

A

small changes to radius have profound changes in flow - smaller radius will decrease blood slow

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22
Q

how does blood vessel length affect flow

A

flow is linearly proportional to length

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23
Q

how does hypertension affect angiotensin

A

increased in hypertension
it is a vasoconstrictor
GF causing SMCs to proliferate and migrate

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24
Q

neurotransmitters in parasympathetic and sympathetic NS

A

p - preganglionic and postganglionic fibres use acetyl choline
s - preganglionic fibres use Ach and post use noradrenaline and adrenaline
sweat glands postganglionic fibres release Ach even in sympathetic NS

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25
Q

how do baroreceptors regulate BP

A

in carotid sinus and aortic arch
high pressure will give high stretch - brain initiates reduction in sympathetic drive to vessels - blood vessel diameter would increase
low stretch will mean low BP - brain increases sympathetic activity - constriction of vessels - increases resistance and so increases pressure

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26
Q

3 NTs expected in any sympathetic nerve (sympathetic triad)

A

neuropeptide y (NPY)
ATP
noradrenaline
needed for fine control and regulation

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27
Q

receptor of NPY in sympathetic nerve

A

y receptor

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28
Q

receptor of noradrenaline in sympathetic nerve

A

alpha and beta adrenoreceptors

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29
Q

receptor of ATP in sympathetic nerve

A

P2x receptor (ion channel)

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30
Q

causes of large vasoconstriction

A

increase sensitivity of receptors
more NT
drive high frequency activation - will release neuropeptide - gives big contraction

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31
Q

where are NTs in a nerve

A

synthesised in cell body, travel down axons
varacosities can take up NT and store them while they wait for release
AP travelling down nerve increases chance of NT release

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32
Q

what is perivascular adipose tissue

A 
PVAT surrounds most large blood vessels and plays an important role in vascular homeostasis
can be pro or anti contractile
removing fat can damage vessel wall
sensory nerves are present 
compounds from fat can influence nerves
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33
Q

what is an electrocardiogram (ECG)

A

a recording of the electrical activity of the heart from the skin

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34
Q

parts of an ECG wave

A

before P - impulse formation in SA node
p - atrial depolarisation
between p and q - delay at AV node while ventricles fill (after atria contraction)
q - conduction through bundle branches and purkinje fibres
qrs - ventricular depolarisation
ST segment - plateau phase of repolarisation - pretty electrically stable
t - final rapid repolarisation

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35
Q

where are the left ad right bundle branches

A

ventricular septum

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36
Q

what are ECG leads

A

not the wire attached to patient

viewpoint we look at activity from - the electrical vector

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37
Q

two types of ECG lead

A

unipolar and bipolar leads

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38
Q

difference between bipolar and unipolar ECG leads

A

unipolar measures the potential variation at a single point

bipolar measures potential difference between two points

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39
Q

unipolar leads

A

augumented limb leads - aVR, aVL, aVF

chest leads - V1-V6

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40
Q

bipolar leads

A

limb leads I, II and III
I = between right arm and left arm
II = RA to left leg
III = LA to LL

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41
Q

inferior ECG leads

A

III, aVF and II

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42
Q

anterior ECG leads

A

V1-4

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43
Q

lateral ECG leads

A

aVL, I, V5-6

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44
Q

systematic approach to an ECG

A 
always ask for clinical context
check the date, time and patient details
access technical quality eg paper speed
identify PQRST
measure HR with QRS
check ECG intervals
determine QRS axis
look at P, QRS, T morphology 
can look at old ECGs to see progression
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45
Q

how to determine HR from ECG

A

300 divided by number of large squares between each QRS complex
1 square = 300/min as 300/1 = 300
2 squares = 150/min as 300/2 = 150
or
number of QRS complexes across ECG (10sec) x6

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46
Q

normal ranges for ECG intervals

A

PR interval - <1 large square, <200ms
QRS - <3 small squares, <120ms
QT interval - <11 small squares, <440ms

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47
Q

what is the QRS axis

A

direction of average depolarisation in heart
determined from limb leads
angle determined relative to lead I
normal is -30 to +90 degrees (+ve QRS in I and II)
axis is approximated by finding lead with most +ve QRS

48
Q

abnormal QRS axis

A

left axis deviation - -30 to -90 degrees - positive QRS in I, negative in II and aVF
right axis deviation - +90 to +180 degrees - negative QRS in I, positive in aVF
extreme axis deviation - negative QRS in I and II, positive in aVR

49
Q

normal P/QRS/T morphology

A

normal P wave is upright in inferior leads
ST segment is flat
T wave has same polarity as QRS

50
Q

pleural effusion

A

build-up of excess fluid between the layers of the pleura outside the lungs

51
Q

indications for using an echocardiogram

A

when structural imaging of one of the following is needed:
left or right ventricle and their cavities
valves
pericardium
atria and septa between cardiac chambers
great vessels

52
Q

what is an echocardiogram

A

type of ultrasound scan

53
Q

difference between a transthoracic and transesophageal echocardiogram

A

Transthoracic - noninvasive, taking place entirely outside your body
Transesophageal - guide a special ultrasound probe into your mouth and down your oesophagus behind LA after sedation - can get better pictures

54
Q

what is a doppler echocardiogram

A

procedure that uses Doppler ultrasonography to examine the heart
the use of Doppler technology allows determination of the speed and direction of blood flow by utilizing the Doppler effect

55
Q

what is cardiovascular resonance

A

CMR scan uses a strong magnetic field and radio waves to create detailed images of the heart
45-60 minute scan

56
Q

when to use CMR

A

ischaemic heart disease, heart failure assessment, myocardial tissue characterisation, valvular heart disease, adult congenital heart disease, reference-standard LV and RV volumes

57
Q

disadvantages of CMR

A

expensive
lengthy examination timwa
claustrophobia
patient co-operation eg for breath holds

58
Q

what is late gadolinium enhancement

A

a technique used in CMR - gadolinium attaches to the scar and shows up white on scan
normally used for the assessment of regional scar formation and myocardial fibrosis

59
Q

what is a CTCA

A

CT of coronary arteries
liquid containing iodine is injected into a vein
iodine increases density of blood in vessels allowing us to see inside and outside of vessels
beta-blockers to slow HR, CT can get imaging during diastole

60
Q

what is a stress test

A

proves or excludes inducible ischaemia in myocardium
exercise or drugs are used if you are unable to exercise
Dobutamine is put in a vein and causes the heart to beat faster - mimics the effects of exercise on the heart
atropine and adenosine can also be used

61
Q

contra-indications of an exercise stress test

A

unable to exercise
uncontrolled hypertension
unstable symptoms

62
Q

pros and cons of a stress echo

A 
pros:
cheap
very few side effects
safe
availability
ischemia and valve assessment
cons:
needs good acoustic window
operator dependent
expertise limited
63
Q

nuclear cardiology

A

uses noninvasive techniques to assess myocardial blood flow, evaluate the pumping function of the heart as well as visualise the size and location of a heart attack
can also be a stress test
resolution not as good as MRI
coloured pictures produced

64
Q

what is a coronary angiography

A

procedure that uses contrast dye, usually containing iodine, and x ray pictures to detect blockages in the coronary arteries that are caused by plaque buildup

65
Q

what do the different colours in an xray mean

A 
air = black
fat = grey
muscle = grey
bone = calcium = white
66
Q

function of pleural cavity

A

fluid filled space that allows lungs to inflate and deflate against chest wall without friction

67
Q

pectus excavatum

A

congenital deformity of the chest wall that causes several ribs and sternum to grow into the thoracic space

68
Q

pectus carinatum

A

genetic disorder of the chest wall, making the chest stick out
happens because of an unusual growth of rib and sternum cartilage - sternum more pertuberant

69
Q

role of diaphragm in breathing

A

diaphragm moving up and down is what causes lungs to inflate and deflate
it contracts causing itself to move down
lungs also move down due to them being in a confined space and this inflates the lungs - air drawn in
then diaphragm relaxes which pushes lungs up and air moves out - deflate
diaphragm separates the thorax from the abdomen

70
Q

causes of diaphragm paralysis

A 
Peripheral - phrenic nerve injury:
iatrogenic - surgery, anesthetic blocks
trauma 
neuropathy
viral 
central:
spinal cord injury
cord compression 
central hypoventilation syndrome
tumors
71
Q

which spinal nerves innervate the diaphram

A

C3, 4, 5

phrenic nerve

72
Q

causes of primary hypertension

A 
smoking
obesity
diet - salt
lack of exercise
genetic
73
Q

complications of chronic hypertension

A 
leads to further cardiovascular disease:
atherosclerosis
stroke - BP higher in cerebral arteries - potential aneurysm 
myocardial infarction 
heart failure
renal failure
retinopathy
74
Q

equation for BP

A

BP = TPR x CO

where TPR = total peripheral resistance

75
Q

lowering BP by drug action

A

block of sympathetic NS:
B1-blockers will reduce the effects on heart and will reduce renin release from the kidney
a1-blockers will reduce effects on blood vessels
kidney:
diuretics will reduce blood volume
hormones:
ACE inhibitors and angiotensin receptor blockers will inhibit the renin-angiotensin-aldosterone system
Ca+ channel blockers will cause vasodilation of peripheral resistance arterioles

76
Q

what are Beta-adrenoceptor blockers and how do they reduce BP

A

competitive reversible antagonists that:
decrease BP via blockade of B1 sympathetic tone on the heart and reduction in renin release from the kidney
decrease HR and SV
decrease CO

77
Q

Beta-adrenoceptor blocker examples

A

propanolol acts on B1 and B2

atenolol is B1 selective

78
Q

adverse effects of beta-adrenoceptor blockers

A

exacerbate asthma - block of B2 means absolute contraindication
intolerance to exercise
hypoglycaemia
vivid dreams

79
Q

examples of alpha-adrenoceptor blockers

A

phentolamine blocks a1 and a2

doxazosin and prazosin are a1 selective

80
Q

what are alpha-adrenoceptor blockers and how do they reduce BP

A

competitive reversible antagonists
they decrease BP via a decrease in sympathetic tone in arterioles (a1)
decease in peripheral resistance

81
Q

adverse effects of alpha-adrenoceptor blockers

A

postural hypotension due to loss of sympathetic venoconstriction
reflex tachycardia via baroreceptors

82
Q

how do ACE inhibitors lower BP

A

reduced formation of the vasoconstrictor angiotensin II (decrease in peripheral resistance)
reduced blood volume (loss of angiotensin II-stimulated release of aldosterone, thus reduction of renal reabsorption of Na+ and water)

83
Q

ACE inhibitor examples

A

captopril and enalapril

84
Q

adverse effects of an ACE inhibitor

A

generally very well tolerated but:
sudden fall in BP on 1st dose
persistent irritant cough - due to reduced bradykinin (normally broken down by ACE), a peptide that activates sensory neurons in lung tissue

85
Q

describe angiotensin II receptor blockers

A

two receptor subtypes: AT1 and AT2
AT1 receptor mediates vasoconstrictor and aldosterone-releasing actions of angiotensin
losartan and candesartan are AT1 blockers

86
Q

how do diuretics lower BP

A

by reducing blood volume
mechanism is through reduced renal reabsorption of Na+ and water
additional vasodilator action may also contribute to decrease in peripheral resistance

87
Q

adverse effect of diuretics

A

decrease in plasma K+

88
Q

function of L-type voltage operated calcium channels

A

open upon membrane depolarisation

calcium entry into cardiac and vascular smooth muscle

89
Q

function of calcium channel blockers

A

reduce Ca2+ entry into vascular smooth muscle and cardiac muscle by blocking L-type voltage-operated calcium channels

90
Q

mechanism of L-type channel block

A

open channel block - like a cork in a bottle - verapamil and diltiazem work this way
allosteric modulation - bind at allosteric site and reduce channel opening by conformation change - nifedipine works this way

91
Q

how do calcium channel blockers reduce BP

A 
reduce peripheral resistance (block of Ca2+ entry into vascular smooth muscle leads to vasodilation)
reduce CO (block of Ca2+ entry into cardiac muscle - HR and SV are both reduced)
92
Q

difference between rate-limiting and non-rate limiting calcium channel modulators

A

non-rate limiting:
more effective vasodilators and more vascular-selective because the exhibit voltage dependent blockade - cardiac conducting cells are relatively hyperpolarised whereas vascular smooth muscle is relatively depolarised
rate-limiting:
have more marked effects directly on the cardiac conduction pathways and cardiac muscle
they slow HR and reduce conduction and contractility

93
Q

adverse effects of L-type blockers

A

headache - dilation of cerebral blood vessels
constipation - relaxation of gastrointestinal smooth muscle
heart block - failure of cardiac myocytes to contract due to decrease Ca2+ concentration
cardiac failure

94
Q

initial step in treating hypertension

A

person aged under 55 gets an ACE inhibitor or low cost angiotensin II receptor blocker
person aged over 55 or black person of African or Caribbean family origin of any age will get a calcium channel blocker

95
Q

beginning of atherosclerosis

A

starts with insult to the vascular endothelium eg smoking, high shear stress, infection diabetes
increased adhesion and transmigration of leukocytes - create oxidant stress
increased permeability to lipids
generation of cytokines/oxidant stress
establishes a focus of inflammation

96
Q

formation of a fatty streak

A

platelet adhesion
migration of smooth muscle cells - PDGF to form fibrous cap
uptake of modified LDLs - LOX-1
formation of lipid-laden foam cells (monocytes-macrophages)
release of MMPs by macrophages
compensatory vessel remodelling

97
Q

advanced lesion in atherosclerosis

A 
formation of fibrous cap-healing
foam cells burst/die and release lipid into necrotic core
necrotic core-lipids debris
further monocyte recruitment
oxidation of LDLs within plaque
98
Q

unstable fibrous plaque

A 
fibrous cap thins 
thrombus formation 
intraplaque haemorrhage
vessel occlusion 
myocardial infarction
99
Q

what makes a plaque vulnerable

A

larger lipid core
thinner fibrous cap
abundance of inflammatory cells
paucity of smooth muscle cells

100
Q

what is cholesterol essential for

A

incorporating into cell membranes
maintaining membrane fluidity and permeability
production of steroids and fat-soluble vitamins

101
Q

how does the liver effect cholesterol levels

A

liver monitors levels of cholesterol
regulates this through synthesis, absorption and bile secretion
drugs to treat hyperlipidaemia target this process in the liver/gut

102
Q

lipoprotein examples

A 
chylomicrons
VLDL
IDL
LDL
HDL
only HDL is good
103
Q

chylomicrons

A

carry triglycerides from intestines to liver, muscle and adipose tissue

104
Q

VLDL

A

carry newly synthesised TGs from liver to adipose tissue

105
Q

IDL

A

an intermediate between VLDL and LDL

106
Q

LDL

A

low density lipoprotein
major reservoir of cholesterol
taken up via LDL receptors by endocytosis

107
Q

HDL

A

high density lipoprotein
adsorb cholesterol released by dying cells
also act as reverse transport to take cholesterol to liver

108
Q

exogenous pathway of cholesterol transport

A

Dietary cholesterol and fatty acids are absorbed.
Triglycerides are formed in the intestinal cell from free fatty acids and glycerol and cholesterol is esterified.
Triglycerides and cholesterol combine to form chylomicrons.
Chylomicrons enter the circulation and travel to peripheral sites.
In peripheral tissues, free fatty acids are released from the chylomicrons to be used as energy, converted to triglyceride or stored in adipose.
Remnants are used in the formation of HDL.

109
Q

how can obesity generate systemic inflammation

A

adipose tissue synthesises inflammatory cytokines

110
Q

endogenous pathway of cholesterol transport

A

VLDL is formed in the liver from triglycerides and cholesterol esters.
These can be hydrolyzed by lipoprotein lipase to form IDL or VLDL remnants.
VLDL remnants are cleared from the circulation or incorporated into LDL.
LDL particles contain a core of cholesterol esters and a smaller amount of triglyceride.
LDL is internalized by hepatic and nonhepatic tissues.
In the liver, LDL is converted into bile acids and secreted into the intestines.
In non hepatic tissues, LDL is used in hormone production, cell membrane synthesis, or stored.
LDL is also taken up by macrophages and other cells which can lead to excess accumulation and the formation of foam cells which are important in plaque formation.

111
Q

familial hypercholesterolaemia

A

a genetic disorder characterised by high cholesterol levels, specifically very high levels of low-density lipoprotein
most common mutations diminish the number of functional LDL receptors in the liver

112
Q

signs of familial hypercholesterolaemia

A

xanthomas - fatty cholesterol-rich deposits on skin, usually around elbows, knees, buttocks and tendons
xanthelasmas - fatty deposits in the eyelids
arcus senilis - a white ring around the cornea

113
Q

hyperlipoproteinaemia

A

high circulating levels of free and bound cholesterol and triglycerides

114
Q

secondary causes of hyperlipoproteinaemia

A

diabetes mellitus, alcoholism, hypothyroidism, liver disease, drugs, diet

115
Q

what are statins

A

HMGCoAR inhibitors
competitive inhibitors of rate limiting step in cholesterol biosynthesis
marked decrease in cholesterol levels may stimulate LDL receptor up-regulation
most effective at night when most cholesterol biosynthesis occurs

phase 2 cardiovascular and respiratory block (5 decks)

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