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Medicine: PBL wrap-ups > Unit 4 Case 2: Supraventricular Tachycardia > Flashcards

Unit 4 Case 2: Supraventricular Tachycardia Flashcards

1
Q

myocardium

A

cardiac muscle

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2
Q

myocardial infarction

A

death of a segment of heart muscle
which follows interruption of its blood supply
also known as a heart attack

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3
Q

cardiac arrest

A

heart stops effectively pumping
presents with abrupt loss of consciousness

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4
Q

symptoms of a myocardial infarction

A

chest pain
deferred pain
light headed or dizzy
sweating
shortness of breath
feeling or being sick
overwhelming feeling of anxiety
coughing or wheezing

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5
Q

different types of heart attack

A

acute coronary syndrome which are
ST segment elevation myocardial infarction
non-ST segment elevation myocardial infarction
unstable angina

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6
Q

treatment for STEMI

A

percutaneous coronary intervention
medications
bypass surgery

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7
Q

treatments for NSTEMI and unstable angina

A

usually medications
coronary angioplasty
coronary artery bypass graft

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8
Q

stent with balloon angioplasty

A

build up of cholesterol partially blocking blood flow through the arteries
stent with balloon interred into partially blocked artery
balloon inflated to expand stent
balloon removed from expanded stent

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9
Q

what is SVT

A

supra ventricular tachycardia
conditions where your heart suddenly beats much faster than normal
some may need treatment
heart rate can suddenly rise to over 100bpm
can happen when resting or exercising
problem occurs in the atria

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10
Q

tachycardia meaning

A

means abnormally rapid heart rhythm

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11
Q

symptoms of SVT

A

episode length may vary from seconds to hours
pulse becomes 140-200
thumping heart sensations, palpations
dizziness or light headed
may become breathless
may feel chest discomfort
if you have angina the angina pain may be triggered by episode of SVT

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12
Q

treatment of SVT

A

may only last a few minutes so no treatment in the case
can change lifestyle to reduce chance of having episodes
if episodes are long you may need hospital treatment such as medicines, cardio version and catheter ablation
may administer dose of adenosine to rapidly restore normal heart rate

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13
Q

what are vagal manoeuvres

A

activate parasympathetic activity
- decrease blood pressure
- decrease heart rate

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14
Q

types of vagal manoeuvres

A

valsalva
cough
gag
knees to chest
cold water treatment
carotid sinus massage

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15
Q

valsalva manoeuvre

A

sit or lie down
take deep breath and hold
pinch nose and close mouth
try to breathe out as hard as possible for 10 to 15 seconds
always first line of treatment in SVT attack

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16
Q

cough

A

must cough hard to generate pressure in your chest and stimulate vagus nerve

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17
Q

gag

A

try with your finger or doctor may use tongue depressor

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18
Q

holding knees against your chest

A

do for a minute
may be best in babies and children

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19
Q

cold water treatment

A

apply ice water to face for approximately 5 seconds
can also immerse face in icy water for several seconds
stepping into cold shower or ice bath may also work

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20
Q

carotid sinus massage

A

only performed by a doctor
lie down and stick out your chin
doctor would put pressure on carotid sinus

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21
Q

drugs used in this case

A

adenosine
propanalol

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22
Q

target of adenosine

A

G protein coupled receptors on neurons

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23
Q

1st effect of adenosines activity

A

adenosine activates A1 receptors found on neurones that keep the brain awake
neurons become less active

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24
Q

2nd effect of adenosines activity

A

adenosine activates A2A receptor that are found on neurons that initiate sleep
these neurons become more active

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25
Q

physiology of adenosine

A

combination of activity of both receptors means weaker wake signal and a stronger sleep signal
makes you feel more refreshed when you wake up
due to less adenosine when you wake up

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26
Q

clinical adenosine

A

given as an IV
used to bring heart rate back to normal rhythm
decreases heart rate
delays action potential in the SAN

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27
Q

side effects of adenosine

A

diarrhoea
feeling warmth
nausea
passing of gas

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28
Q

target and classification of propanalol

A

beta blocker
target is the B receptors on the cardiac myocyte cell

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29
Q

propranolol mechanism of action

A

blocks B1 receptor on the cardiac myocyte cell
inhibits adenylate cyclase enzyme
inhibits AMP synthesis
reduces production of PKA
decrease in calcium influx through ion channels

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30
Q

physiology of propranolol

A

decrease in sympathetic effect
decrease in heart rate and contractility

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31
Q

clinical propanalol

A

heart problems because
reduces high blood pressure
helps prevent chest pain
used to treat irregular heart rates
used to treat anxiety

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32
Q

how does stress affect your heart rate

A

stress causes the release of hormone adrenaline
adrenaline increases your heart rate and blood pressure
in order to cope with the stressful situation

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33
Q

how does sleep deprivation affect your heart rate

A

lack of sleep increases daytime heart rate
increases stress hormone norepinephrine which can constrict blood vessels and increase blood pressure

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34
Q

how does caffeine affect your heart rate

A

promotes release of noradrenaline and norepinephrine to increase heart rate and blood pressure

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35
Q

how does alcohol affect your heart rate

A

at the time of drinking can cause a temporary increase in heart rate and blood pressure
in long term drinking able guidelines can lead to on-going increased heart rate, high blood pressure, weakened heart muscle and irregular heartbeat

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36
Q

blood flow physiology

A

SVC/IVC/cornary sinus
right atrium
tricuspid valve
right ventricle
pulmonary valve
pulmonary artery
lungs
pulmonary vien
left atrium
mitral valve
left ventricle
aortic semi lunar valve
aorta
body

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37
Q

pulmonary circulation

A

low pressure system
right side of heart pumps deoxygenated blood through pulmonary circulation to collect oxygenn

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38
Q

systemic circulation

A

high pressure system and more resistance
left side of the heart pumps oxygenated blood to systemic circulation

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39
Q

3 stages of a single heartbeat

A

partial depolarisation
ventricular depolarisation
atria and ventricular depolarisation

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40
Q

electrical conduction system of the heart

A

SA node: natural pacemaker. Releases electrical stimuli at regular rate. Each stimulus passes through myocardial cells of Atria creating a wave of contraction that spreads rapidly though both atria ​
Electrical stimulus from SA node reaches AV node + briefly delayed so that contracting atria have enough time to pump all the blood into ventricles. Once atria empty of blood, atrioventricular valves close. At this point atria begin to refill + electrical stimulus passes through AV node + Bundle of His into bundle branches + purkinje fibres​
All cells in ventricles receive electrical stimulus causing them to contract + blood leaves them​
At this point ventricles are empty, atria are full, atrioventricular valves are closed. SA node is about to release another electrical stimulus + process is about to repeat itself. BUT SA + AV node contain only 1 stimulus, so every time nodes release a stimulus, they must recharge before they can do it again.​
SA node recharges whilst atria are refilling, AV node recharges whilst ventricles are refilling. There’s no need for a pause in heart function. ​
Depolarisation: release of an electrical impulse​
Repolarisation: recharging of an electrical impulse ​

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41
Q

3 stages of the cardiac cycle

A

atrial systole
ventricular systole
diastole

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42
Q

atrial systole

A

contraction of the atria
AV valves open so blood enters the ventricles

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43
Q

ventricular systole

A

contraction of the ventricles
AV valves shut and the semi-lunar valves open so blood leaves the heart through great arteries

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44
Q

diastoole

A

relaxation of the atria and the ventricles

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45
Q

what makes the lub sound

A

S1
tricuspid/mitral valve closing

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46
Q

what makes the dub sound

A

S2
aortic and pulmonic valve closing

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47
Q

when do valves open

A

when pressure is higher in the chamber before the one the blood is leading ro

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48
Q

when do valves close

A

when the pressure of the chamber before the valve is lower than that of the chamber the blood is flowing through
preventing the backflow of blood

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49
Q

systolic blood pressure

A

pressure in the arteries when ventricles squeeze out blood under high pressure

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50
Q

diastolic blood pressure

A

when ventricles fill up with blood under lower pressure

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51
Q

cardiac output

A

amount of blood pumped out by the ventricles over a period of time

52
Q

venous return

A

rate at which veins return blood back to the atria

53
Q

what is cardiac output equal to

A

venous return

54
Q

stroke volume

A

volume of blood ejected from the heart in one cardiac cycle

55
Q

equation for stroke volume

A

EDV - ESV in ml

56
Q

cardiac output equation

A

cardiac output (mL/min) = stroke volume mL x heart rate (bpm)

57
Q

what is an ECG

A

electrocardiogram
used to check heart rhythm and electrical activity
sensors attached to the skin and used to detect the electrical signal produced by your heart every time it beats
signals are recorded by a machine

58
Q

symptoms of a possible heart problem

A

chest pain
palpitations
dizziness
shortness of breath

59
Q

what can an ECG help to detect

A

arrhythmias
coronary heart disease
heart attacks
cardiomyopathy

60
Q

arrhythmias

A

where the heart beats too slowly, quickly or irregularly

61
Q

coronary heart disease

A

where the hearts blood supply is blocked or interrupted bu a build up of fatty substances

62
Q

heart attacks

A

where the supply of blood to the heart is suddenly blocked

63
Q

cardiomyopathy

A

where the hearts walls become thickened or enlarged

64
Q

how is an ECG carried out

A

generally attach a number of small sticky sensors called electrodes to arms legs and chest
connected by wires to an ECG machine
need to remove upper clothing and chest needs to be shaved and cleaned

65
Q

3 main types of ECG

A

resting
stress or exercise
ambulatory/ holter monitor

66
Q

resting ECG

A

carried out whilst you’re lying down in a comfortable position

67
Q

stress or exercise ECG

A

carried out whilst using an exercise bike or a treadmill

68
Q

ambulatory ECG

A

electrodes connected to a small portable machine worn at your waist so your heart can be monitored at home for one or more days

69
Q

what are the sections that will be shown on an ECG

A

p wave
pr interval
QRS complex
ST segment
T wave

70
Q

P wave

A

atrial contraction

71
Q

PR interval

A

time taken for excitation to spread form SAN across the atrium and down to the ventricular muscle via the bundle of His

72
Q

QRS

A

ventricular contraction

73
Q

ST segment

A

ventricular relaxation

74
Q

T wave

A

ventricular depolarisation

75
Q

normal duration of Pr interval

A

0.12-0.2 seconds
3-5 small squares

76
Q

QRS normal duration

A

<0.12 seconds
3 small squares

77
Q

normal duration of QRS

A

0.38-0.42 seconds

78
Q

normal adult heart rate

A

60-100 bpm

79
Q

tachycardia heart rate

A

> 100 bpm

80
Q

bradycardia heart rate

A

< 60 bpm

81
Q

if a patient has a regular heart rhythm how can their heart rate be calculated on an ECG

A

count number of large squares within one R-R interval
divide this number by 300

82
Q

how to calculate a patients heart rate if the rhythm is irregular

A

count number of complexes on the rhythm strip, normally 10 seconds long
multiply complexes by 6

83
Q

what can irregular rhythms be

A

regularly irregular
irregularly irregular

84
Q

regularly irregular

A

recurrent pattern of irregularity

85
Q

irregularly irregular

A

completely disorganised

86
Q

patients heart rhythm on ECG

A

mark several R-R intervals on paper
move them along the rhythm strip to check if subsequent intervals are similar

87
Q

checking for P waves in heart rhythm

A

are they present
are they followed by a QRS complex
do they look normal, check duration time and shape
if they are absent is there any atrial activity

88
Q

what is in the image and what does it mean

A

sawtooth baseline
flutter waves

89
Q

what is in the image and what does it mean

A

chaotic baseline
fibrillation waves

90
Q

flatline

A

no atrial activity

91
Q

prolonged PR interval

A

create than 0.2 seconds
suggests the presence of atrioventricular delay/ AV block

92
Q

types of AV block

A

first degree
second degree type 1
second degree type 2
third degree

93
Q

PR interval shortened

A

p wave originating from closer to the AV node
conduction takes less time
atrial impulse getting to the ventricle by faster shortcut instead of conducting slowly across atrial wall
accessory pathway can be associated with delta wave

94
Q

what should you look at regarding QRS complex

A

width
height
morphology

95
Q

narrow QRS complex

A

<0.12 seconds
the impulse is conducted down the bundle of his and purkinje fibres to ventricles
well organised synchronised ventricular depolarisation

96
Q

broad QRS complex

A

> 0.12 seconds
abnormal depolarisation sequence
e.g. ventricular ectopic where impulse spreads slowly across myocardium
atrial ectopic narrow QRS
bundle branch block as impulse gets to one ventricle rapidly down intrinsic conduction then spreads slowly across myocardium to other ventricle

97
Q

small QRS complex

A

<5mm in limb leads and <10 mm in chest leads

98
Q

tall QRS complexes

A

ventricular hypertrophy
can be due to body habits e.g. tall slim people

99
Q

morphology

A

assess the individual waves of the QRS complex
delta wave
sign that the ventricles are being activated earlier than normal form point distant to the AV node
early activation spreads slowly across myocardium causing slurred upstroke of QRS complex
associated with Wolff Parkinson white but required evidence of tachyarrythmias and delta wave to be diagnosed

100
Q

Q waves

A

isolated can be normal
pathological is >25% size of R wave that follows or >2mm in height and >40ms in width
look for Q waves in entire territory for evidence of previous MI

101
Q

R and S waves

A

assess R wave progression across chest leads V1 to V6
transition S> R to R> S occurs in V3 or V4
poor progression can be sign of MI or poor lead position

102
Q

J point

A

where the S wave joins the ST segment
can be elevated resulting in ST segment that is raised
high take off is normal variant

103
Q

key points for assessing the j point segment

A

benign early depolarisation occurs mostly under the age of 50
typically J point is asked with widespread ST elevation in multiple terrorise making ischaemia less likely
T waves are also raised
ECG abnormalities don’t change, during STEMI changes will evolve and on benign early depolarisation will remain same

104
Q

ST segment

A

should be isoelectric line

105
Q

ST elevation

A

significant when greater than 1 small square in 2 or more continuous limb leads or >2mm in 2 or more chest leads
most commonly caused by acute full thickness MI

106
Q

ST depression

A

ST depression ≥ 0.5 mm in ≥ 2 contiguous leads indicates myocardial ischaemia.

107
Q

tall T waves

A

T waves are considered tall if they are:
> 5mm in the limb leads AND
> 10mm in the chest leads (the same criteria as ‘small’ QRS complexes)
Tall T waves can be associated with:
Hyperkalaemia (“tall tented T waves”)
Hyperacute STEMI

108
Q

inverted T waves

A

T waves are normally inverted in V1 and inversion in lead III is a normal variant.
Inverted T waves in other leads are a nonspecific sign of a wide variety of conditions:
Ischaemia
Bundle branch blocks (V4-6 in LBBB and V1-V3 in RBBB)
Pulmonary embolism
Left ventricular hypertrophy (in the lateral leads)
Hypertrophic cardiomyopathy (widespread)
General illness
Around 50% of patients admitted to ITU have some evidence of T wave inversion during their stay.
Observe the distribution of the T wave inversion (e.g. anterior/lateral/posterior leads).

109
Q

biphasic T waves

A

Biphasic T waves have two peaks and can be indicative of ischaemia and hypokalaemia.

110
Q

flattened T waves

A

Flattened T waves are a non-specific sign, that may represent ischaemia or electrolyteimbalance.

111
Q

u waves

A

U waves are not a common finding.
The U wave is a > 0.5mm deflection after the T wave best seen in V2 or V3.
These become larger the slower the bradycardia – classically U waves are seen in various electrolyte imbalances, hypothermia and secondary to antiarrhythmic therapy (such as digoxin, procainamide or amiodarone).

112
Q

what is in the image

A

SVT
refers to any tachydysrhythmia arising from above the level of the Bundle of His, and encompasses regular atrial, irregular atrial, and regular atrioventricular tachycardias
In the absence of aberrant conduction (e.g. bundle branch block). The ECG will demonstrate a narrow complex tachycardia

113
Q

what may indicated an MI on an ECG

A

pathological Q waves
St segment changes (elevation)

114
Q

what do the following ECG changes show:
poor R wave progression
ST segment elevation
T wave inversion

A

MI in the anterior wall
affecting leads V2 to V4
involving the left anterior descending artery, diagonal branch

115
Q

what do the following ECG changes show:
R wave disappears
ST segment rises
T wave inverts

A

MI in the septal wall
affecting leads V1 and V2
involving the left anterior descending artery, septal branch

116
Q

what do the following ECG changes show:
ST segment elevation

A

MI in the lateral wall
affecting leads I, aVL, V5 and V6
involving the left coronary artery, circumflex branch

117
Q

what do the following ECG changes show:
T wave inversion
ST segment elevation

A

MI in the inferior wall
affecting leads 2,3, aVf
involving the right coronary artery, poster descending branch

118
Q

what do the following ECG changes show:
tall R waves
ST-segment depression
Upright T waves

A

MI in the posterior wall
affecting leads V1 to V4
involving left coronary artery, circumflex branch and the right coronary artery, posterior descending branch

119
Q

reading ECG paper

A

small square is 0.04 seconds
large square is 0.2 seconds
5 large squares is 1 second
300 large squares is 1 minute

120
Q

what does the ST segment represent

A

time between depolarisation and repolarisation of the ventricles
ventricular contraction

121
Q

RR interval

A

begins at the peak of one R wave and ends at the peak of the next R wave
represents the time between two QRS complexes

122
Q

Qt interval

A

begins at the start of the QRs complex and finishes at the end of the T wave
represents the time taken for the ventricles to depolarise and then repolarise

123
Q

effects of stress on the body

A

fatigue
headaches
taut muscles
skin irritations
frequent infections
constricted breathing

124
Q

effects of stress on the mind

A

worrying
indecision
negativity
foggy thinking
hasty decisions
impaired judgement

125
Q

effects of stress on behaviour

A

substance abuse
loss of appetite
accident prone
restlessness
loneliness
insomnia

126
Q

effects of stress on emotions

A

loss of confidence
apprehension
indifference
depression
irritability
insomnia

127
Q

risk factors for anxiety in medical and dental students

A

economic difficulties
loss of close relatives
long study hours
competition
no time for extracurriculars

Medicine: PBL wrap-ups (21 decks)

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