Unit 4 Case 2: Supraventricular Tachycardia Flashcards
(127 cards)
1
Q
myocardium
A
cardiac muscle
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
3
Q
cardiac arrest
A
heart stops effectively pumping
presents with abrupt loss of consciousness
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
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
6
Q
treatment for STEMI
A
percutaneous coronary intervention
medications
bypass surgery
7
Q
treatments for NSTEMI and unstable angina
A
usually medications
coronary angioplasty
coronary artery bypass graft
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
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
10
Q
tachycardia meaning
A
means abnormally rapid heart rhythm
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
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
13
Q
what are vagal manoeuvres
A
activate parasympathetic activity
- decrease blood pressure
- decrease heart rate
14
Q
types of vagal manoeuvres
A
valsalva
cough
gag
knees to chest
cold water treatment
carotid sinus massage
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
16
Q
cough
A
must cough hard to generate pressure in your chest and stimulate vagus nerve
17
Q
gag
A
try with your finger or doctor may use tongue depressor
18
Q
holding knees against your chest
A
do for a minute
may be best in babies and children
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
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
21
Q
drugs used in this case
A
adenosine
propanalol
22
Q
target of adenosine
A
G protein coupled receptors on neurons
23
Q
1st effect of adenosines activity
A
adenosine activates A1 receptors found on neurones that keep the brain awake
neurons become less active
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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physiology of adenosine
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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clinical adenosine
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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side effects of adenosine
diarrhoea
feeling warmth
nausea
passing of gas
28
target and classification of propanalol
beta blocker
target is the B receptors on the cardiac myocyte cell
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propranolol mechanism of action
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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physiology of propranolol
decrease in sympathetic effect
decrease in heart rate and contractility
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clinical propanalol
heart problems because
reduces high blood pressure
helps prevent chest pain
used to treat irregular heart rates
used to treat anxiety
32
how does stress affect your heart rate
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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how does sleep deprivation affect your heart rate
lack of sleep increases daytime heart rate
increases stress hormone norepinephrine which can constrict blood vessels and increase blood pressure
34
how does caffeine affect your heart rate
promotes release of noradrenaline and norepinephrine to increase heart rate and blood pressure
35
how does alcohol affect your heart rate
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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blood flow physiology
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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pulmonary circulation
low pressure system
right side of heart pumps deoxygenated blood through pulmonary circulation to collect oxygenn
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systemic circulation
high pressure system and more resistance
left side of the heart pumps oxygenated blood to systemic circulation
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3 stages of a single heartbeat
partial depolarisation
ventricular depolarisation
atria and ventricular depolarisation
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electrical conduction system of the heart
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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3 stages of the cardiac cycle
atrial systole
ventricular systole
diastole
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atrial systole
contraction of the atria
AV valves open so blood enters the ventricles
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ventricular systole
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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diastoole
relaxation of the atria and the ventricles
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what makes the lub sound
S1
tricuspid/mitral valve closing
46
what makes the dub sound
S2
aortic and pulmonic valve closing
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when do valves open
when pressure is higher in the chamber before the one the blood is leading ro
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when do valves close
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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systolic blood pressure
pressure in the arteries when ventricles squeeze out blood under high pressure
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diastolic blood pressure
when ventricles fill up with blood under lower pressure
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cardiac output
amount of blood pumped out by the ventricles over a period of time
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venous return
rate at which veins return blood back to the atria
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what is cardiac output equal to
venous return
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stroke volume
volume of blood ejected from the heart in one cardiac cycle
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equation for stroke volume
EDV - ESV in ml
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cardiac output equation
cardiac output (mL/min) = stroke volume mL x heart rate (bpm)
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what is an ECG
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
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symptoms of a possible heart problem
chest pain
palpitations
dizziness
shortness of breath
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what can an ECG help to detect
arrhythmias
coronary heart disease
heart attacks
cardiomyopathy
60
arrhythmias
where the heart beats too slowly, quickly or irregularly
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coronary heart disease
where the hearts blood supply is blocked or interrupted bu a build up of fatty substances
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heart attacks
where the supply of blood to the heart is suddenly blocked
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cardiomyopathy
where the hearts walls become thickened or enlarged
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how is an ECG carried out
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
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3 main types of ECG
resting
stress or exercise
ambulatory/ holter monitor
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resting ECG
carried out whilst you're lying down in a comfortable position
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stress or exercise ECG
carried out whilst using an exercise bike or a treadmill
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ambulatory ECG
electrodes connected to a small portable machine worn at your waist so your heart can be monitored at home for one or more days
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what are the sections that will be shown on an ECG
p wave
pr interval
QRS complex
ST segment
T wave
70
P wave
atrial contraction
71
PR interval
time taken for excitation to spread form SAN across the atrium and down to the ventricular muscle via the bundle of His
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QRS
ventricular contraction
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ST segment
ventricular relaxation
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T wave
ventricular depolarisation
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normal duration of Pr interval
0.12-0.2 seconds
3-5 small squares
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QRS normal duration
<0.12 seconds
3 small squares
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normal duration of QRS
0.38-0.42 seconds
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normal adult heart rate
60-100 bpm
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tachycardia heart rate
>100 bpm
80
bradycardia heart rate
< 60 bpm
81
if a patient has a regular heart rhythm how can their heart rate be calculated on an ECG
count number of large squares within one R-R interval
divide this number by 300
82
how to calculate a patients heart rate if the rhythm is irregular
count number of complexes on the rhythm strip, normally 10 seconds long
multiply complexes by 6
83
what can irregular rhythms be
regularly irregular
irregularly irregular
84
regularly irregular
recurrent pattern of irregularity
85
irregularly irregular
completely disorganised
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patients heart rhythm on ECG
mark several R-R intervals on paper
move them along the rhythm strip to check if subsequent intervals are similar
87
checking for P waves in heart rhythm
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
what is in the image and what does it mean
sawtooth baseline
flutter waves
89
what is in the image and what does it mean
chaotic baseline
fibrillation waves
90
flatline
no atrial activity
91
prolonged PR interval
create than 0.2 seconds
suggests the presence of atrioventricular delay/ AV block
92
types of AV block
first degree
second degree type 1
second degree type 2
third degree
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PR interval shortened
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
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what should you look at regarding QRS complex
width
height
morphology
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narrow QRS complex
<0.12 seconds
the impulse is conducted down the bundle of his and purkinje fibres to ventricles
well organised synchronised ventricular depolarisation
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broad QRS complex
> 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
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small QRS complex
<5mm in limb leads and <10 mm in chest leads
98
tall QRS complexes
ventricular hypertrophy
can be due to body habits e.g. tall slim people
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morphology
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 waves
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
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R and S waves
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
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J point
where the S wave joins the ST segment
can be elevated resulting in ST segment that is raised
high take off is normal variant
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key points for assessing the j point segment
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
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ST segment
should be isoelectric line
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ST elevation
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
ST depression
ST depression ≥ 0.5 mm in ≥ 2 contiguous leads indicates myocardial ischaemia.
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tall T waves
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
inverted T waves
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).
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biphasic T waves
Biphasic T waves have two peaks and can be indicative of ischaemia and hypokalaemia.
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flattened T waves
Flattened T waves are a non-specific sign, that may represent ischaemia or electrolyteimbalance.
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u waves
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
what is in the image
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
what may indicated an MI on an ECG
pathological Q waves
St segment changes (elevation)
114
what do the following ECG changes show:
poor R wave progression
ST segment elevation
T wave inversion
MI in the anterior wall
affecting leads V2 to V4
involving the left anterior descending artery, diagonal branch
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what do the following ECG changes show:
R wave disappears
ST segment rises
T wave inverts
MI in the septal wall
affecting leads V1 and V2
involving the left anterior descending artery, septal branch
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what do the following ECG changes show:
ST segment elevation
MI in the lateral wall
affecting leads I, aVL, V5 and V6
involving the left coronary artery, circumflex branch
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what do the following ECG changes show:
T wave inversion
ST segment elevation
MI in the inferior wall
affecting leads 2,3, aVf
involving the right coronary artery, poster descending branch
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what do the following ECG changes show:
tall R waves
ST-segment depression
Upright T waves
MI in the posterior wall
affecting leads V1 to V4
involving left coronary artery, circumflex branch and the right coronary artery, posterior descending branch
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reading ECG paper
small square is 0.04 seconds
large square is 0.2 seconds
5 large squares is 1 second
300 large squares is 1 minute
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what does the ST segment represent
time between depolarisation and repolarisation of the ventricles
ventricular contraction
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RR interval
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
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Qt interval
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
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effects of stress on the body
fatigue
headaches
taut muscles
skin irritations
frequent infections
constricted breathing
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effects of stress on the mind
worrying
indecision
negativity
foggy thinking
hasty decisions
impaired judgement
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effects of stress on behaviour
substance abuse
loss of appetite
accident prone
restlessness
loneliness
insomnia
126
effects of stress on emotions
loss of confidence
apprehension
indifference
depression
irritability
insomnia
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risk factors for anxiety in medical and dental students
economic difficulties
loss of close relatives
long study hours
competition
no time for extracurriculars
