CARDIOLOGY Flashcards
what is the most common cause of mitral stenosis
rheumatic fever
Hypoglycaemia with impaired GCS
give IV Glucose if there is access- 100 ml of 20%
Management of hypoglycaemia
In patients with hypoglycaemia causing a low GCS, the BNF advises IV glucose administration if there is IV access. An alternative is IM glucagon - not IV glucagon. In this instance, the patient has IV access and so the STAT dose of IV glucose can easily be administered. If the GCS was not impaired, than proprietary products of quick-acting carbohydrate such as GlucoGel® can be given or alternatively the above-mentioned soft drinks.
What calcium channel blocker should never be prescribed with a beta blocker
verapamil - has rate limiting effects, so if prescribed with BB can cause complete heart block
first line management for angina
beta blocker or ccb
gtn
statin
what medication for angina do patients become tolerant to
nitrites
what is De Musset’s sign
head bobbing with aortic regurge
changes to NICE hypertension guidelines
lowering the threshold for treating stage 1 hypertension in patients < 80 years from 20% to 10%
angiotensin receptor blockers can be used instead of ACE-inhibitors where indicated
if a patient is already taking an ACE-inhibitor or angiotensin receptor blocker, then a calcium channel blocker OR a thiazide-like diuretic can be used. Previously only a calcium channel blocker was recommended
what ecg change can hypokalaemia cause
long qt
what are the acquired causes of long qt
Electrolyte imbalance: hypokalaemia, hypocalcaemia and hypomagnesaemia
Medications: in addition to those listed in the subject notes below: tramadol, metoclopramide and domperidone.
CNS lesions: subarachnoid haemorrhage and ischaemic stroke
Malnutrition
Hypothermia
drugs that cause long qt
amiodarone, sotalol, class 1a antiarrhythmic drugs tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram) methadone chloroquine terfenadine** erythromycin haloperidol ondanestron
First line anti hypertensive for diabetes pt
ACE inhibitor
Causes if aortic dissection
Marfans HTN Bicuspid aortic valve Pregnancy Traumatic injury Atherosclerosis (calcium deposits in aorta) High intensity weight lifting
Signs of aortic dissection on CXR
Widened mediastinum
Calcification of aorta
Double layer in aorta (calcification and then blood where dissection has occurred)
Covid
What does a small and large square represent time wise on an ecg
Small square = 0.04 s
Large square = 0.2 s
what length of time does the rhythm strip at the bottom of ecg show
10 s
how can you quickly calculate hr from ecg
300/ number of big squares
count the number of QRS across rhythm strip and x by 6 as it is 10s
what is a normal range for corrected QT for men and women
men = 0.45 women = 0.47
what do the ecg waves represent - from p, qrs, t
- P wave - atrial depolarisation
- Q wave - septal left side first deflection
- R wave - septal (early ventricular) depolarisation
- S wave - circumference (late ventricular) depolarisation
- T wave - ventricular repolarisation
how does a posterior infarct look om ecg
st depression in v1 and 2
method for reviewing an ecg
rate rhythm axis (reaching inwards R, leaving L) segments - st (character) waves - p and t (bipid p waves, tall tented t waves) intervals - pr, qrs, qt (time)
what 10 rules should you check in an ecg
PR interval should be 120 - 200ms. 3-5 little squares
QRS should not be more than 120 ms, <3 small squares
QRS should be dominantly upright in leads I and II
QRS and T waves should have the same general direction in the same limb lead
All leads are negative in aVR.
The R wave must from V1 to at least V4; S wave must grow from V1 - V3, and disappear in V6
ST segment should start isoelectric, expect in V1 and V2 where it may be elevated
P waves should be upright in I, II and V2 - V6
There should be no q wave or small q wave, less than 0.04 in I, II, v2-v6
T wave must be upright in I, II, v2-v6.
signs of ischemia on ecg
ST depression, t wave inversion
signs of hyper acute MI
Tall (giant) T waves
what do bifid p waves show (p mitrale)
left atrial enlargement
what do tall p waves show (p pulmonale)
right atrial enlargement
what does a short PR interval indicate
WPW - accessory pathway
what does a long PR interval indicate
1st degree heart block
how deep is a pathological q wave
> 2 mm
How can you look for BBB, how can you work out which side it is on
Look in precordial leads (chest leads)
Look at V1 - the defection will tell you if its L or R
Look if it is widened
If it is widened and has a positive deflection in V1 = RBBB bc the later RV depolarisation (via current from LV) is moving towards V1 electrode = positive
If it is widened and has a negative deflection in V1 = LBBB bc the later LV depolarisation is moving away from V1 electrode
How can an MI show on an ecg
Giant T waves
ST elevation
LBBB
ST depression - anteroseptal leads (V1-4) - posterior
How can an MI show on an ecg
Giant T waves
ST elevation
LBBB
ST depression - anteroseptal leads (V1-4) - posterior (also possibly ?posterior infarct with inferior ST depression)
What are the causes of BBB
- Ventricular strain - PE, RHF, COPD (RBBB), Valve disease (AS - LBBB)
- Vascular - Ischemia/ infarct - MI - LBBB
What BBB is most commonly associated with an MI
LBBB
What is a hemi block on ecg
When the QRS is not widened
What is a bifasicular block, and causes
When 2 of the 3 conducting pathways are blocked
LBBB is always bifasicular
RBBB plus anterior or posterior hemiblock is a bifasicular block
How can you tell right and left ventricular hypertrophy on ecg
R - look in R leads V1, V2 - S+R >10
L - look in L leads V5, V6 - S+R >45
What is a delta wave
J-like sloping where Q wave should be
Sign of aberrant pathway
What is an epsilon wave
Wave that shows R ventricular dysplasia/ cardiomyopathy
What is an osborne or ‘J wave’
Sign of hypothermia
PE ECG trace
s1, q3, t3
What is brugada syndrome
What are symptoms
What are changes on ecg
Genetic disorder affecting sodium channels
Can cause arrhythmias at rest and during sleep
Symptoms - syncope/ blackouts
ECG changes 3 types:
type 1 - ST elevation V1 - sharks tail
type 2 - saddle v2,3
type 3 - saddle v2,3
How does hypertrophic cardiomyopathy look on ecg
LVH changes (large R waves) plus T wave inversion and st segment depression
List some ecg findings with coronary artery disease
Pathological (>2mm) Q waves ST depression T wave inversion and peaking BBB AV block
what is the definition of st elevation on ecg
ST elevation >1 mm in 2 limb leads next to each other
ST elevation >2mm in 2 precordium leads next to each other
Explain the temporal ecg changes that occur with myocardial ischemia
J segment depression (where S meets isoelectric line)
ST depression
ST elevation
U wave inversion
Explain the temporal ecg changes that occur with myocardial infarction (transmural)
Peaked/ giant t waves (minutes) ST segment elevation/ progression (mins - hours) Loss of R wave (hours - days) T wave inversion (days) T wave normalisation (weeks to months)
how many leads should a q wave be in
2 or more
Infarct of which coronary artery can affect the SA and AV nodes
right coronary
what are the different classes of antiarrhythmics
I - sodium blockers
II - beta blockers
III - K+ blockers
IV - calcium blockers
pharmacological management of tachycardia in acute heart failure
never beta blockers
can use digoxin if need to - negative inotrope, positive chronotrope
what should you never use in acute heart failure
beta blockers
what should you consider when prescribing digoxin
kidney function
can overdose if have ckd as need dose adjustments
what is the half life of amiodarone, what does this mean clinically
around 50 days
need high loading doses
what is the effect of amioderone on the liver
it is an enzyme inhibitor so it can prevent other medicines from being metabolised
eg when prescribed with digoxin, digoxin dose must be halved
what arrhythmia can amiodarone cause
long qt
should not be prescribed with other medicines that can cause long qt
combination of which two cardio drugs can cause AV block
Beta blockers and verapamil
what is the definition of sinus bradycardia
HR <60 bmp
what drug can be given for sinus bradycardia
atropine
what drugs can cause AV block
Beta-blockers
Rate limiting calcium-channel blockers (e.g. diltiazem, verapamil)
Digoxin
List some of the causes of AV block
Cardiomyopathy Conduction system fibrosis Connective tissue disease Hypothyroidism Ischaemic heart disease Radiotherapy Sarcoidosis
explain first, second and third degree AV block
first = long PR interval (atria)
second = mobitz type 1 is when there is increasing PR interval then the QRS drops (AV node)
type 2 is when the QRS drops randomly - usually in a certain ration eg 3:1 (bundle of his)
third = no relationship between p and qrs (below AV node) - if QRS is narrow escape rhythm has come from just below AV node, if wide from further down in ventricles
describe an approach to differentiate different tachyarrhythmias
- is the qrs regular, if irregular = AF
- is qrs narrow or broad - narrow above AV, wide below
- P wave morphology and P:R ratio
P waves normal and P:R 1:1 = sinus tachycardia
P waves abnormal and P:R 1:1 = focal atrial tachycardia
no p waves = AVRT or AVNRT
p wave rate >250 = flutter
P:R 2:1 or greater = re-entrant tachy with AV block
what drug management should you give to an unstable patient with a tachy arrhythmia
Intravenous adenosine (providing there is no contraindication) at a dose of 6 mg, then if no effect 12 mg, then if no effect a further 18 mg (maximum total dose of 36 mg). This should temporarily lead to AV blockade and so provide more information regarding the underlying rhythm (e.g. is there underlying AF?)
what are the main drugs associated with long QT
Macrolide antibacterials (e.g. erythromycin), many antipsychotics and tricyclic antidepressants have all been associated with a prolonged QT. Baseline ECGs are often recommended.
In which patients is flecanide contraindicated in
ischaemic heart disease or known structural cardiac abnormalities
list some contraindications to cardioversion
Contraindications to anticoagulants
Structural heart disease
Permanent AF (usually more than 12 months)
A history of multiple failed attempts are/or relapses even with concomitant use of antiarrhythmics or non-pharmacological approaches
An ongoing but reversible cause of AF
which cardiac drugs can induce AV block
antiarrhythmics
