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csi (phase 1b) > case 15 - well man check > Flashcards

case 15 - well man check Flashcards

1
Q

what is the NHS Health Check?

A

a free check-up of your overall health

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2
Q

what does the NHS health check involve?

A

tell you whether you’re at higher risk of getting certain health problems over the next 10 years and how to reduce your risk of them

  • heart disease
  • diabetes
  • kidney disease
  • stroke
  • dementia (above 65)
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3
Q

what is calculated in the NHS health check and why is that useful?

A

your individual cardiovascular risk calculated and explained

given advice on how to prevent cardiovascular conditions (tailored, personalised advice)

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4
Q

what happens at an NHS health check?

A

takes approx 20-30 mins

healthcare professional (nurse/HCA) will

  • ask you questions about your lifestyle and family history
  • measure height and weight
  • take blood pressure
  • do a blood test (to assess risk of CVD, stroke, kidney disease, diabetes etc)
  • give you personalised advice to improve your risk
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5
Q

what personalised advice is given to improve your risk at an NHS health check?

A
  • how to improve your diet and the amount of physical activity you do
  • taking medicines to lower your blood pressure or cholesterol
  • how to lose weight or stop smoking
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6
Q

where do NHS health checks take place?

A

at a GP surgery or local pharmacy

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7
Q

how are NHS health checks arranged?

A

usually invited every 5 years if you’re between 40 and 74 years of age and do not already have a pre-existing condition

local authority can send appointment letters to invite you as well

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8
Q

do NHS health checks work?

A

for every 30 to 40 people having an NHS Health Check, 1 person is diagnosed with high blood pressure

for every 80 to 200 people having a Health Check, 1 person is diagnosed with type 2 diabetes

for every 6 to 10 people having an NHS Health Check, 1 person is identified as being at high risk of cardiovascular disease

= have prevented around 2500 heart attacks or strokes in the first five years

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9
Q

how can hypertension affect the brain?

give two possible effects

A

transient ischaemic attack

stroke

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10
Q

how can hypertension affect the eyes?

give two possible effects

A

hypertensive retinopathy

optic neuropathy

(glaucoma)

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11
Q

how can hypertension affect the heart?

give two possible effects

A

left ventricular hypertrophy

angina

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12
Q

how can hypertension affect the kidneys?

give two possible effects

A

glomerulosclerosis

kidney failure

(chronic kidney disease)

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13
Q

how can hypertension affect the peripheral vasculature?

give two possible effects

A

atherosclerosis

aneurysm

(peripheral vascular disease)

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14
Q

how is hypertension managed?

(according to the NICE guidelines)

A

recheck BP

24 hour ambulatory BP monitoring

lifestyle advice

recheck BP

start medication

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15
Q

what is 24-hour ambulatory blood pressure monitoring (ABPM)?

A

a method to measure blood pressure on a continuous basis

= gives a more accurate picture of your blood pressure

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16
Q

when is 24hr ABPM carried out?

A

to identify untreated patients who have high BP readings in the clinic but normal readings during usual daily activities outside of this setting (‘white coat hypertension’)

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17
Q

how is 24hr ABPM carried out?

A

small digital blood pressure monitor is attached to a belt around your waist and connected to a cuff around your upper arm

blood pressure is measured as you move around, living your normal daily life

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18
Q

in which scenarios is ABPM most useful?

A

in scenarios where white coat hypertension is suspected

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19
Q

what lifestyle recommendations are made for patients with hypertension?

A

weight loss

increased physical activity

dietary modifications

reduced salt intake

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20
Q

what is salt-sensitive hypertension and how common is it?

A

changes in blood pressure levels parallel to change in salt intake

= around 30-50% of hypertensive patients

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21
Q

what is white coat hypertension?

A

when the blood pressure readings at your doctor’s office are higher than they are in other settings

= when readings are over 140/90mmHg in clinic and under this threshold normally at home

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22
Q

what do the NICE guidelines suggest for all people diagnosed with hypertension?

A
  • test for proteinuria, estimated ACR (albumin:creatinine ratio), haematuria
  • blood test for HbA1c. electrolytes, eGFR, total cholesterol and HDL cholesterol
  • 12-lead ECG
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23
Q

what is the P wave of an ECG linked to?

A

atrial depolarisation (triggered by the SAN)

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24
Q

what is the P-R segment of an ECG linked to?

A

the delay caused when the electrical impulse slows down as it travels from the SAN to the AVN to allow time for ventricular filling

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25
Q

what is the QRS complex of an ECG linked to?

A

ventricular depolarisation

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26
Q

what is the T wave of an ECG linked to?

A

repolarisation of the ventricles

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27
Q

why is the T wave positive if it is measuring repolarisation (opposite direction)?

A

goes in the same direction

= measuring it as negative charge already
(the last cells to depolarise are the first cells to repolarise)

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28
Q

why is the amplitude of the waves on an ECG different?

(e.g. R wave compared to T wave)

A

reflects the amount of muscle that has ongoing electrical activity which varies

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29
Q

why is the T wave smaller than the R wave if the amplitude is a measure of muscle mass involved?

A

T wave is more spread out that R wave

(depolarisation occurs over a shorter period of time whereas repolarisation takes longer)

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30
Q

what takes longer on an ECG: depolarisation OR repolarisation and why?

A

repolarisation takes longer as it does not utilise the cardiac His-Purkinje conduction system, unlike depolarisation AND instead, repolarisation relies on cell-to-cell conduction

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31
Q

why is it called a 12-lead ECG when you are placing only 10 electrodes?

A

put simply, a lead is like a perspective

in a 12-lead ECG, there are 10 electrodes providing 12 perspectives of the heart’s activity using different angles

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32
Q

name the electrodes in an ECG

A

limb electrodes = RA, LA, RL, LL

chest electrodes = V1, V2. V3, V4, V5, V6

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33
Q

where are the limb electrodes placed during an ECG?

A

RA (red) = right shoulder OR right wrist

LA (yellow) = left shoulder OR left wrist

RL (black) = right thigh OR right ankle

LL (green) = left thigh OR left ankle

= preferably over bone rather than muscle

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34
Q

where are the chest electrodes placed during an ECG?

A

V1 = 4th ICS, right sternal border

V2 = 4th ICS, left sternal border

V3 = between V2 and V4

V4 = 5th ICS, mid-clavicular line

V5 = 5th ICS, anterior axillary line

V6 = 5th ICS, mid-axillary line

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35
Q

what views do the standard, bipolar limb leads reflect on an ECG?

A

lead I = lateral

lead II = inferior

lead III = inferior

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36
Q

what views do the augmented, unipolar limb leads reflect on an ECG?

A

aVR = N/A

aVL = lateral

aVF = inferior

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37
Q

what views do the precordial, unipolar chest leads reflect on an ECG?

A

V1 = septal

V2 = septal

V3 = anterior

V4 = anterior

V5 = lateral

V6 = lateral

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38
Q

what are the artery territories on an ECG?

A
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39
Q

what does the following ECG suggest?

A

normal ECG, unremarkable

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40
Q

how is an ECG interpreted?

A

confirm patient’s details

calibration

rate, rhythm, axis

assess actual ECG:
- P waves (use rhythm strip, V1)

  • P-R interval (length normally 3-5 squares, elongated? gradual elongation? missing beats?)
  • QRS complex (1:1 ratio; amplitude; regular/irregular missing QRS complex, width)
  • ST segment (isoelectric; elevation, depression)
  • QT interval (may have a QTc corrected value)
  • T wave (present after every QRS; inverted, present/absent, other waves e.g. U waves)
  • pacemaker spikes, other abnormalities?
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41
Q

how do you assess P waves on an ECG?

A

use rhythm strip or V1

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42
Q

how do you assess P-R intervals on an ECG?

A

!! length normally 3-5 squares !!

elongated?

gradual elongation?

elongation and dropping QRS complexes?

= possible heart blocks

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43
Q

how do you assess QRS complex on an ECG?

A

1:1 ratio w P waves?

amplitude

regular/irregular missing QRS complex

width

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44
Q

how do you assess S-T segments on an ECG?

A

isoelectric?
elevated?
depressed?

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45
Q

how do you assess Q-T intervals on an ECG?

A

may have a QTc corrected value

= corrected for heart rate

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46
Q

how do you assess T waves on an ECG?

A

present after every QR?

inverted?
present?
absent?

other waves can also appear e.g. U waves

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47
Q

interpret the following ECG

A 
rate = approx 50bpm (sinus bradycardia)
rhythm = normal
axis = normal

1) QRS complex = huuuge increase in height IN V1-V6 (much larger voltages + overlap each other)
2) ST segment = elevated in V1-V4 (in line w abnormal repolarisation - not an MI, no other symptom)
3) T wave = inverted T wave in V5-V6 (abnormal repolarisation)

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48
Q

what does the height of a QRS complex indicate?

A

the mass of cardiac muscle present

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49
Q

what does a significantly increased QRS complex height (voltage) indicate?

A

significantly increased cardiac muscle

= left ventricular hypertrophy

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50
Q

what is the most obvious feature of left ventricular hypertrophy on an ECG?

A

no gaps between the QRS complexes + significant overlap between them

= indicates huge increase in cardiac muscle mass
= left ventricular hypertrophy

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51
Q

what do inverted T waves indicate?

A

abnormal repolarisation

in the case of LVH
= musculature of heart will be abnormal
= repolarise abnormally

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52
Q

what does ST elevation normally indicate?

A

myocardial infarction

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53
Q

without the presentation of any other cardiac symptoms, what can ST elevation indicate?

A

can add to the diagnosis of the patient

(in this case, of left ventricular hypertrophy)

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54
Q

differentiate between l left ventricular hypertrophy and ischaemia

A

left ventricular hypertrophy = increased thickness of cardiac muscle of the left ventricle

ischaemia = lack of blood supply

LVH can lead to ischaemia as the blood supply can be inadequate for the increased muscle mass

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55
Q

explain the pathophysiology of hypertensive cardiomyopathy

A

hypertension

= increased afterload + increased peripheral vascular resistance
= increased cardiac activity and pressure overload
= pressure and volume mediated left ventricular remodelling to compensate for the increased demand for cardiac activity
= upregulation of angiotensin, aldosterone, endothelin release
= LVH leads to left ventricular dilation
= hypertensive cardiomyopathy

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56
Q

how is hypertensive cardiomyopathy managed?

A

take action (medication, lifestyle changes) to slow progression

as disease cannot be reversed

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57
Q

what is hypertensive cardiomyopathy?

A

hypertensive (hight blood pressure) that causes cardiomyopathy (abnormal heart muscle)

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58
Q

explain how hypertension leads to reduced ejection fraction

A

hypertension
= increased afterload + increased peripheral vascular resistance
= increased cardiac activity and pressure overload
= pressure and volume mediated left ventricular remodelling to compensate for the increased demand for cardiac activity
= LV becomes way more stiff + pressure in the LV raised
= interferes w diastolic function
= can lead to systolic dysfunction as stiffness impairs blood being pumped out
= reduced ejection fraction

59
Q

what happens as a result of increased volume overload on the heart?

A

heart has to accommodate for increased circulating volume

= left ventricular dilatation

60
Q

differentiate between dilation and dilatation

A

dilation describes the passive enlargements whereas dilatation describes active enlargements

61
Q

which antihypertensive drugs are chosen for patients with hypertension and type 2 diabetes?

A

step 1: ACEi / ARB

step 2: ACEi / ARB + CCB / diuretic

step 3: ACEi /ARB + CCB + diuretic

(keep checking before every escalation whether there is still a need to prescribe the drug)

62
Q

which antihypertensive drugs are chosen for patients with hypertension and without type 2 diabetes?

A

step 1: CCB

step 2: CCB + ACE i/ ARB

step 3: CCB + ACEi/ARB + diuretic

(keep checking before every escalation whether there is still a need to prescribe the drug)

63
Q

why are some hypertensive patients given CCBs whereas others are given ARBs/ACEis?

A

individuals that have salt-sensitive hypertension (reduced responsiveness to renin) respond better to CCBs than ARB/ACEis

64
Q

how is the administration of any medication begun?

A

begin with lowest dose

check health status of patient/response

if needed, uptitrate to higher dose

65
Q

how do calcium channel blockers work?

A

preferentially block L-type calcium channels on vascular smooth muscle

decrease in calcium entering vascular smooth muscle

= decreased actin-myosin cross-bridge formation
= reduced frequency and strength of contraction
= vasodilation of vasculature
= reduced hypertension

66
Q

what are the two types of calcium channel blockers?

A

DHP (dihydropyridine)
non-DHP (non-dihydropyridine)

67
Q

differentiate between the two types of CCBs

A

more potent vasodilators than non-dihydropyridine (non-DHP) agents

but non-DHP have more marked ionootropic effects

68
Q

why may blood pressure be raised despite the administration of an antihypertensive drug?

A

reduced patient adherence with drug (do you find it easy to take your drugs? do you take it on most days?)

side effects

multiple drugs required for intensity of symptoms

ethnicity

white-coat syndrome

69
Q

why may blood pressure be raised despite the administration of an antihypertensive drug?

A
  • reduced patient adherence with drug (do you find it easy to take your drugs? do you take it on most days?)
  • side effects
  • multiple drugs required for intensity of symptoms
  • ethnicity
  • white-coat syndrome
70
Q

what are the possible causes of non-adherence with medication?

A

no proper education on how/when to take it

side effects

interactions with other drugs

71
Q

which cells control the electrical activity of the heart?

A

pacemaker cells (of the SAN)

72
Q

why are pacemaker cells said to be autorhythmic?

A

can continually self-generate new action potentials that go out to the rest of the heart

73
Q

how do pacemaker cells vary compared to skeletal muscle cells?

A

pacemaker cells = independent action potential generation to stimulate contraction

skeletal muscle cells = receive action potential signals from other neurones to stimulate contraction

74
Q

explain how charges sit in depolarisation

A

normally, cells more positive outside then inside (resting membrane potential = -70mV)

but depolarisartion is when the inside cell becomes more positive than normal

75
Q

which pacemaker cells in the SAN fire to stimulate contraction?

A

for each contraction, one pacemaker cell out of the group will randomly and automatically depolarize first

but each contraction will be led by a different cell of the pacemaker group

76
Q

what is Bachmann’s bundle and why is it important?

A

an atrial internodal tract

= connect the SAN to spots in the right and left atria, so there can be coordinated atrial depolarisation to push blood simultaneously into the ventricles

77
Q

what does Bachmann’s bundle allow?

A

transmission of electrical impulses from the right atrium to the left atrium

= to allow for coordinated atrial depolarisation and contraction

78
Q

as well as to the left atrium, where else does the depolarisation wave travel?

A

from the SAN to the AVN

79
Q

why does the conduction velocity slow down in the AVN? (2)

A
  • the AV nodal cells have very small diameters which increases resistance to electrical flow
  • they use the relatively slower opening calcium ion channels rather than the faster opening sodium ion channels for depolarisation
80
Q

explain what a depolarisation wave is

A

adjacent cells depolarising one after the other

the depolarisation of one cell stimulates the depolarisation of the next cell and so on

81
Q

why is the delay in conduction at the AVN physiologically important?

A

depolarisation stimulates muscle contraction so the delay in conduction delays depolarisation allowing proper ventricular filling before ventricular contraction

= ensure good stroke volume & cardiac output

82
Q

why is the AVN important?

A

only location in the heart where electrical impulses can travel from the atria to the ventricles

83
Q

describe the electrical conduction system of the heart

A
  • SAN
    (via internodal tracts/Bachmann’s bundle)
  • AVN/right atria
  • bundle of His
  • right & left branched bundles
  • Purkinje fibres
84
Q

how does the conduction velocity vary within the conduction system of the heart?

A

at SAN = 1 m/s

at AVN = slows down significantly to 0.01-0.05 m/s

at His-Purkinje system = faster than at the SAN at 2-4 m/s

85
Q

why is it physiologically important that the His-Purkinje system conducts the depolarisation quickly?

A

makes the ventricles contract in a coordinated way

86
Q

what are the other pacemaker cells collectively known as?

A

latent pacemaker cells

ectopic pacemaker/focus

(pace being set for another spot besides the normal SAN spot)

87
Q

when would the ectopic pacemaker cells set the pace?

A

if the SAN pacemaker cells fail, the atrial pacemaker cells take over

if those fail, the AVN pacemaker cells take over

if those fail, then the ventricular pacemaker cells take over

88
Q

define cardiac conduction velocity

A

the velocity at which a depolarisation wave moves through the myocardium

(measured in m/s)

89
Q

what are the units of cardiac conduction velocity?

A

measured in m/s

90
Q

how much time does one depolarisation wave take to travel from the SAN to the Purkinje fibres?

A

200ms

91
Q

explain how the depolarisation wave moves from one cell to the next

A

when ions like calcium and sodium slip through gap junctions and trigger voltage-gated sodium channels in that cell over to open up, allowing a rush of more sodium into the cell and causing an action potential to occur

= horizontal leakage of causes furthering of the action potential

92
Q

what determines the speed of the depolarisation wave?

A

more sodium channels + gap junctions speed up the depolarisation wave

fewer gap junctions + fewer sodium channels slow down the depolarisation wave

93
Q

what is the conduction velocity in the SAN?

A

approx 1 m/s

94
Q

what is the conduction velocity in the AVN and why?

A

approx 0.01-0.05 m/s

= slows down significantly to allow proper, complete ventricular filling before ventricular contraction

95
Q

what is the conduction velocity in the His-Purkinje system and why?

A

approx 2-4 m/s

= increased speed allows for more coordinated ventricular contraction

96
Q

which two factors determine cardiac conduction velocity?

A
  • gap junctions between adjacent cells
  • voltage-gated sodium channels on the cells
97
Q

what is the benefit of being able to see different views of the heart?

A

makes it easier to see how the wave of depolarisation moves through the heart

98
Q

which leads are the septal leads and which coronary artery are they linked to?

A

V1, V2

= left anterior descending artery (LAD)

99
Q

which leads are the anterior leads and which coronary artery are they linked to?

A

V3, V4

= left anterior descending artery (LAD)

100
Q

which leads are the lateral leads and which coronary artery are they linked to?

A

V5, V6, lead I, aVL

= left circumflex artery (LCx)

101
Q

which leads are the inferior leads and which coronary artery are they linked to?

A

lead II, lead III, aVF

= right coronary artery

102
Q

what is the view of the leads like in both the transverse and coronal planes?

A 
coronal = limb leads
transverse = chest leads
103
Q

summarise the following picture

A

depolarisation wave moving towards an electrode as a positive deflection

wave moving away as a negative deflection

(each is proportional to the size of the dipole)

104
Q

why does the lead II vector usually the vector of choice for analysis?

A

depolarisation wave moves from the SA node towards the apex of the heart, so it aligns with the lead II vector

105
Q

heart muscles have a functional syncitium - what does this mean?

A

each cell has its own cell membrane BUT also have tiny connections or openings between them (so they are connected)

= allow the horizontal influx of ions to stimulate the opening of voltage-gated ion channels to cause depolarisation

106
Q

what are the two speeds at which the depolarisation wave moves through the heart?

A

in pacemaker cells = moves really fast

in normal cardiac myocytes = moves much slower

107
Q

what does an ECG measure on the x-axis?

A

time on the X-axis, where one small box is 0.04 s

108
Q

what does an ECG measure on the y-axis?

A

voltage on the Y-axis, with each small box being 0.1 mV

109
Q

what is 0mV on an ECG?

A

isoelectric line

110
Q

what is the P wave representative of?

A

positive deflection that signifies atrial depolarisation

(in the direction of the lead II vector)

111
Q

what is the P wave representative of?

A

positive deflection that signifies atrial depolarisation

(in the direction of the lead II vector)

112
Q

how does the delay in conduction at the AVN show up on an ECG and why?

A

as there is no depolarization wave moving towards or away from lead II during the delay, shows up as a flat line

= P-R interval

113
Q

what is the Q wave?

A

the initial negative deflection of the QRS complex

114
Q

what is the Q wave representative of?

A

as well as going through the faster pacemaker cells, the electrical signal also goes through the normal myocytes of the intraventricular septum

= in a direction away from the lead II vector so slight negative deflection

115
Q

what is the P-R interval representative of?

A

the delay in conduction at the AVN while proper ventricular filling takes place

116
Q

what is the S wave?

A

first downward deflection of the QRS complex that occurs after the R wave

117
Q

what is the S wave representative of?

A

apex of heart depolarises first but wave moves back up to depolarise the top of the ventricles = direction away from lead II

= negative deflection

118
Q

what does the QRS complex represent?

A

ventricular depolarisation

119
Q

what is the J point?

A

the exact point at which the ECG wave hits the isoelectric line following the S wave

120
Q

what is the ST segment?

A

flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave

121
Q

what is the ST segment representative of?

A

a brief period of time following ventricular depolarisation when there is no change in electrical activity

122
Q

why is repolarisation a positive deflection on an ECG?

A

in this case, a wave of ‘negative’ (rather than positive) charge is being measured

123
Q

what is the T wave indicative of?

A

ventricular repolarisation

(atrial repolarisation usually does not show on an ECG)

124
Q

despite repolarising more of the heart, why is the T wave smaller than the QRS complex?

A

repolarisation takes longer then depolarisation so the wave on the ECG is more spread out over time

125
Q

despite repolarising more of the heart, why is the T wave smaller than the QRS complex?

A

repolarisation takes longer than depolarisation so the wave on the ECG is more spread out over time

126
Q

what is the extent of the P-R interval?

A

spans from the beginning of the P wave to the beginning of the QRS complex

127
Q

what does the P-R interval indicate?

A

represents the time from the beginning of atrial depolarisation to the beginning of ventricular depolarisation

128
Q

how long is the P-R interval normally?

A

normally 0.12-0.20 seconds

(3-5 small ECG boxes)

129
Q

what are some scenarios in which the P-R interval can change and how?

A

decrease
- if an irritable atrial pacemaker cell outside the SAN caused depolarisation + it was closer to the AVN

increase

  • if the irritable atrial focus was further away from the AVN
  • first-degree heart block (slows conduction through AVN)
130
Q

what is the normal time span of a QRS complex?

A

normally less than 100 milliseconds or two and a half little boxes

131
Q

what are some scenarios in which the QRS complex is wider and how?

A

if an irritable ventricular cell triggers the depolarisation wave instead of the AVN

= can prolong the QRS time as the wave moves more slowly from one cell to the next rather than through the cardiac conduction system

132
Q

what does a QRS width of 100-120 milliseconds indicate?

A

intermediate QRS complex

133
Q

what does a QRS width of greater than 120 milliseconds indicate?

A

prolonged QRS complex (three small boxes)

134
Q

where does the QT interval span?

A

spans from the beginning of the QRS complex to the end of the T-wave

135
Q

what does the QT interval represent?

A

represents ventricular systole all the way from depolarisation to repolarisation

136
Q

what are normal QT interval readings for a person with a heart rate of 60bpm?

A

440 milliseconds in men

460 milliseconds in women

137
Q

why are QT interval readings dependent on heart rate?

A

QT interval changes depending on the rate

= so cannot really use 60bpm values to compare

138
Q

how does QT interval change with rate?

A

as heart rate increases, QT interval decreases

= less time spent in ventricular systole as the heart beats more in said given time period

139
Q

what is the QTc?

A

when the QT intervals are corrected for the specific heart rate in question to work our if it is prolonged or shorter than expected (compared to the reference QT values at 60bpm)

140
Q

how is the corrected QT interval calculated?

A

Bazzett’s formula

QTc = QT (ms) / (square root of the RR interval (s)/1 second)

141
Q

when would the QT interval be prolonged?

A

due to medications such as amiodarone = antiarrhythmic effects

due to inherited long-QT syndromes (mutations in LQT1-LQT3)

142
Q

what is a complication of prolonged QT intervals?

A

a ventricular tachycardia called ‘torsade de pointes’

= can lead to sudden cardiac death

143
Q

how does a prolonged QT interval lead to torsades de pointes?

A

malfunction of ion channels

impaired/delayed ventricular repolarisation

= triggers a characteristic ventricular tachyarrhythmia

144
Q

name the intervals and segments of an ECG wave

A

csi (phase 1b) (8 decks)

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