Cardiology Flashcards
What are three reversible precipitants of complete heart block?
Non reversible
reversible
* hyperkalaemia
* MI
* drugs - calcium channel blockers/beta blockers
Non
* * cardiac fibrosis
* * infiltratve disease
how do you manage complete heart block
seek and treat precipitant
medical - adrenaline 25-50mcg bolus, isoprenaline infusion 0.1-1mcg/kg/min
Surgical - transcutaneous pacing with analgesia/sedation
disposition - cardiology for pacemaker
What’s the criteria for Brugada
What clinic features must be present for Brugada
List 10 high risk features of chest pain
Prolonged or repetitive pain
Raised biomarkers
ECG changes – ST depression >0.5mm / TWI >2mm
transient ST elevation
VT
Shock
Syncope
DM
Renal failure
PCI 6/12 or CABG ever
EF <40%
What clinical features (5) make VT more likely than SVT
- Age over 35
- IHD
- Structural heart disease
- Previous MI
- CCF
- FH of sudden cardiac dearh
What old ECG make SVT with aberrance more likely than VT
- previous ECGs show bundle branch with identical morphology to
- previous ECGs show WPW (short PR, delta wave, narros QRS)
- previous tachyarrhtymias terminated with vagal or adenosine
What are the 5 ECG features suggesting VT over SVT
- A - Axis - northwest axis
- B - Broad complexes over 200ms
- C - Concordance - positive/negative concordance in leads v1 - v6
- D - Dissociation - is there any AV dissocation - suggestive of VT
1. * P and QRS different rates
2. Capture beats or fusion beats
3. RSR with tall left rabbit ear - E- Early part of QRS is slow - in RBBB right is taller
https://litfl.com/wp-content/uploads/2018/08/ECG-VT-Taller-left-rabbit-ear.jpg
describe main ECG features
What is it?
bradycadia
av dissociation
peaked t waves
broad complex escape
complete heart block with ventricular escape
In an inferior STEMI what lead placement suggest right ventricular infarct
ECG in a kid - describe it
What is it?
What is the management>
tachy - say rate
narrow complex
no p waves
normal R R
Supraventricular tachycardia
Management
Simple - ice park on face
Adenosine 100/200/300mcg/kg
DC cardiversion under sedation - 1 then 2 j/kg
What measures can be used to reduce time to PCI?
ambulance pre notification
immediate ECG on arrival for all those with chest pain
immediate senior doctor review
minimise transfers eg stay on trolley
on number to activate lab
transfer packs
chest pain
1) whats the diagnosis with supportive ECG findings
2) What is the most important complication
1) inferior lateral STEMI
ST elevation in 2,3 AVF
reciprical changes 1 and avl
lateral st depression
q wave in 3
2) monomophic VT
Treament for MI
Analgesia - titrated opiates
aspirin 300mg
clopidogrel (300) or ticagrelor (180mg)
Clexane
cardio input for PCI
only oxygen if sats under 90 - aim for 94-98
What is the pharmacological treatment for monomorphic VT?
Amioderone 5mg/kg
Lidocaine 1-2mg/kg
soltalol 1mg/kg
describe and interpret ECG
What advice would you give to ambos on the phone
- hyperacute T waves anterolateral (de winters)
- upsloping ST v3-v6
- ST elevation 1 and avl
- ST depression 3 and avf
Proximal LAD stenosis
Advice
give stemi meds
analgesia
sats 92-96
inform cath lab
in STEMI what fibrinolytics can be used?
Retaplase 10 units IV now and in 30 mins
Alteplase:
>65kg - 15mg IV then 50mg over 30 mins then 35mg over an hour
<65 15mg IV then 0.75mg/kg over 30 mins and 0.5mh/kg over an hour
what are the absolute/relative contraindicatins to fibronolytics in MI
Absolute
* any prior ICH
* ischaemic stroke in last 3 months
* intercranial malignancy
* suspected aortic dissection
* AV malformation
* Active bleeding
* prior streptokinase in last 6 month (if giving this)
Relative
* poorly controlled severe hypertension
* BP over 180 at presentation
* ischamic stoke over 3 months
* pregnancy
* active peptic ulcer
* surgery within last 3 weeks
what consitutes a failure of MI thrombolysis suggesting need for rescue PCI
persistant pain
failure to reduce ST elevation by 50-75% 90 mins post therapy
what does this show?
junctional rhythm - pacing come from AV node or bundle of his
no p waves or buried in QRS
Describe and interpret
inferior ST elevation
borderline upright T waves V1
St depression v2
Q waves
Inferior STEMI
What initial investigations may you do with ischamic ECG and why?
Troponins - marker of cardiac cell distress
ECHO - to show all abnormalities
CXR - any signs of failure
posterior leads ecg - any posterior signs
What are the clinical findings of APO?
bilateral crackles
widespread wheeze
raised JVP
peripheral oedema
SOB
hypoxia
tachycardia
What can precipitate APO?
hypertension
cardiac ischaemia
renal failure
stress - takutsobos
medicine non compliance
non compliance fluid restriction
inhaltion injury
drowning injury
pancreatitis
acute valve dysfunction
acure arrythmia
What are the treamtents and end points for APO?
**GTN infusion **5-100mcg/min - 30% reduction in htn to reduce preload. decrease WOB and hypoxia
**CPAP **Peep 5 - decrease WOB and hypoxia
Frusemide - reduce BP and WOB
how does CPAP work in APO
reduced pre load by limited SVC/IVC flow to right side of heart
improves gas exchange in alveolar
interpret and describe
Rapid Af with accessory pathway, likely WPW
charecteristics:
irregularly, irregular broad complex
tachycardia
delta waves V3
what is this
delta wave - WPW
diagnosis
Three supporting features
VT
broad complex tachycardia at 180
capture beats
What can cause VT?
- cardiac ischaemia
- electrolytes - hypomag/kalaemia
- drugs - tricyclics
- cardiomyopathes
- sarcoid/amyloid
What are the mangement steps for VT with signs of failure?
- sedate - 25mcg fent
- pads and shock 150-200j
- correct underlying cause
diagnosis and describe abnormality
rhythm irregularly irregular = AF
variable ventricular rate approx 200-250
LAD
2 types of QRS
delta waves V4
AF with accesory pathway
what is the main abnormality?
atrial flutter with 2:1 block, no ischamia
With AF/Flutter, what factors favour rate control v rhythm control?
Rate
* Over 65
* asymptomatic
* longstanding AF
* Left atrial enlargment
Rhythm
* young
* severe symptoms
* short duration
* HF due to AF
* mild or moderate left atrial enlargement
what factors must you consider for long term anticoagulation for AF?
HASBLED score
Hypertension
abnormal liver or renal function
Stroke hx
bleeding hx
Labile INR
over 65
drugs - aspirin/steroids
diagnosis
Why?
monomorphic VT
broad complex tachycardia
NW axis
jeffersons notch
What is a DDD pacemaker and how does it function?
Dual chamber pacemaker
Dual chamber sensing
Dual chamber pacing
dual response to sensing that will inhbiit or trigger pacing depending on underlying rhythm
Describe ECG
- broad complex tachycardia approx 120 with pacing spike before every complex
- absence of p wave suggesting the pacemaker is not triggerd by atrial sensing
- like of atrial spike suggestng pacemaker does not trigger atrium
differntials for someone with a pacemker and tachycardia and lightheadedness.
Management?
- pacemaker mediated tachycardia - reentry tachycardia created by pacemaker
- sensor induced tachycardia - misfire eg from loud noises or vibrations
- lead displacement dystrhymia
Management:
1. urgent pacemaker interrogation
2. magnet overpacemaker to inhibit sensing and stop pacemaker mediated tachy
3. vagal/adenosine or verapamil can inhibit PMT
4. cxr for lead placement
5. check electrolytes
what are the key findings of ECG relevant to her presentation?
Diagnosis?
mangement?
findings:
paced rhythm at 130
pacing spikes after qrs
retrograde p in 1, v1, v5,v6
Diagnosis likely pacemaker mediated tachycardia
Management
cardiac montoring and defib pads
titraite analgesa 25mcg fent
fluid for MAP over 65/70
sats over 94
magnet
chat to cardio
how does a magnet aid in pacemaker dysfunction?
converts to asynchronous pacing which turns off sensing of the pacemaker and allows pacing of atrium and ventricles asynchronously
what are the criteria for cardioversion in AF?
- haemodynamic instability
- patient choice
- onset within 48 hours
- lack of known structural heart disease
- non chronic AF
What score can you use from thrombus risk in af?
CHADVAS
what is the most significant finding?
ST elevation of 2mm followed by negative T wave in V1/V2 or coved ST in V1/V2
causes and management of non arrythomogenic cardiogenic shock
Diagnosis and supportive findings
complete heart block
ECG changes
* broad complex qrs
* av dissocation
* different atrial and ventricular rates
what does this ecg suggest and why?
triple vessel disease/proximal LAD stenosis
Why
ST elevation AVR and multi lead ST depression - this means subendocardial ischaemia
What is this and why?
LBBB meeting scarbossa therefore STEMI equivalent
Why:
LBBB with broad QRS and LAD
hyperacute T waves V2-V4
concordant ST elevation in 1 and avl
Discordant ST elevation V2/V3
non reproducible chest pain in young person:
1. Diagnosis
2. why
3. What further investigations are needed?
Acute pericarditis
Why:
PR depression and diffuse ST elevation no adherant to territory
Investigations
Trop
Echo
MRI
what is this?
what drugs can cause it?
torsades de points
Drugs:
* tricyclics
* organophosphates
* antihistamines
* antifungals
* erythromycin
* class 1 (Na - lidocaine) and class 3 (K - amioderonne) anti arrthtymics
Relevant findings
What can cause this?
extreme brady then polymorphic VT
R on T causing TDP
ventricular ectopics
Causes:
hypok/mag
drugs causing QT prolongation
cardiac ischaemia
list 4 abnormalities
bradycardia at 45
sinus arrhtymia
LAD
RBBB
bifascicular
1st degree block
list organ, sign and investigation of hypertensive end organ damage
list two classes of medictions and doses for hypertensive emergency
what is this view?
apical four chamber
What are the CXR features of APO
main findings
sinus
PR prolongation
QT prolongation
no ischamiea
bradycardia
collapse:
describe abnormalities and their significance
RBBB/LAD - bifascicular block
significant because complete heart block may have occured
list 5 differentials
Cardogenic shock causes:
ACS
arrhyhtmia eg new AF
pericardial tamponade
MV prolapse
LV rupture
non cardiogenic
PE
severe anaemia - GI bleed
Sepsis
justify some bedside investigations
doesnt get better and think synptons due to CAD. Stepwise approach to management
endpoints for resus
repeat ecg - dynamic changes
VBG - shock (lactate) or anaemia
CXR - URTI/pneumothorax
US - LV rupture, tampanade, MV prolapse
management
1. 5ml/kg small boluses
2. ionotropes - adrenanaline 0.04mcg/kg
3. Arrange PCI
end points
BP over 100
urine output over 0.5ml/kg/hr
resolution of lactate/Hb etc
