Cardiology 2 Flashcards
Management of aortic dissection
-
-
- eg of drug
Stanford Type A- ascending aorta (2/3 of cases)
surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention
Stanford Type B- descending aorta, distal to left subclavian origin (1/3 cases)
conservative management
bed rest
reduce blood pressure IV labetalol to prevent progression
Investigations in aortic dissection
CXR what do you see?
If stable-
- key finding:
If unstable-
CXR- Widen mediastrinum
If stable- CT angiography of the chest, abdomen and pelvis
- key finding: false lumen is a key finding in diagnosing
If unstable- Transoesophageal echocardiography (TOE)
Management steps of HF
First line
Second Line
Remember adding this can cause…
Can add in….
Third line (4 med options)
a- criteria (2)
b- criteria (1)
c- especially in who?
d- especially in who?
1 non-medical option!! criteria (1)
First line: ACEi + B-blocker
Second Line: + Sprinolactone
Hyperkalaemia: Because ACEi and Sprinolactone are K+ sparing
Add in… SGLT2 Inhib -flozins
Third line (4 options)
a) Ivabradine
criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%
b) sacubitril-valsartan
criteria: left ventricular fraction < 35%
is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
should be initiated following ACEi or ARB wash-out period
c) digoxin
digoxin has also not been proven to reduce mortality in patients with heart failure. It may however improve symptoms due to its inotropic properties
it is strongly indicated if there is coexistent atrial fibrillation
d) hydralazine in combination with nitrate
this may be particularly indicated in Afro-Caribbean patients
cardiac resynchronisation therapy
indications include a widened QRS (e.g. left bundle branch block) complex on ECG
Stable patient, AF with a broad complex tachy will indicate what?
Atrial fibrillation with bundle branch block is the most likely cause of an irregular broad complex tachycardia in a stable patient
STEMI criteria - 2 continuous/ adjacent leads with…
- > 2.5mm (2.5 small sqaures) ST elev. in leads V2-V3 in men < 40years or 2mm ST elev in V2-3 in men. 40 years
- 1.5 mm elev in V2-3 in women
- 1mm ST elev in other leads
- new LBBB (WiLLiaM- V1 W, V6- M)
other cause of increased pro-BNP other than HF?
Renal dysfunction (eGFR < 60) can cause a raised serum natriuretic peptides
if no HF signs and poor CKD then it’ll be the CKD and breathlessness will be anaemia
Talk through how you interpret and ECG: 11 steps and their lengths
- Patient details
- Rate
- Rhythm- irreg or reg?
- Sinus- p waves and QRS following
- Anything grossly abnormal- ST elevation
- Axis deviation
- PR interval (0.12- 0.2s therefore 3-5 squares!)
- QRS (< 3 small sqaures 0.12s)
- ST segment
- QT interval- 0.4s (10 small squares)
- T wave inversion
what class is carvediol?
What is the rule for adding sprinolcatone or a/B-blocker in HTN?
Beta blocker
K + < 4.5 - sprinolcaonte
K + > 4.5 - alph or beta block
Side effect of b blocker-
What anti-anginal drug can cause perforated GU ulcers?
B-blocker = E.D (cock blocker)
Nicorandil
Half life of adenosine
10s therefore SE are quick
Management of Wolf-Park White
definitive-
medical (3 options)
Def- radiofrequency ablation of the accessory pathway
medical
- sotalol***, amiodarone, flecainide
sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation
Infective endocarditis
what valve affected the most?
Rheumatic fever
IE
- If IV drug user- Tricuspid
- If previously normal valves then Mitral
Rh- Mitral
Bradycardia peri-arrest management
1. 1st line
2. can repeat up to..
3.
4.
5. specialist advice for…
- 1st line- Atropine 500mcg IV
- repeat up to 3mg
- Transcutaneous pacing/ external pacing
- Adrenaline/ isoprenaline IV
- Specialist advuse for transvenous pacing
ADENOSINE
how does adenosine have to be given?
1.
2
3. with…
avoid in (1 and why?)
what drug enhances it?
what drug blocks it?
What is the MOA of the drug and what receptor does it act on?
-
-
large calibre (16G) or central route
give over 2 seconds followed by 30ml NaCl 0.9% or can be diluted with NaCl
avoid:
-asthmatics due to bronchospasm
enhances- dipyridamole (anti-platelet)
blocks- theophylline
MOA
- Agonist of A1 receptor in AVN and induces a temporary heart block in AVN
Side effects:
- flushing
- chest pain/ SOB/ impeding doom
- bronchospasm
Investigations of stable angina
1st
2nd
3rd
examples of 2nd line (2/4)
1st- CT contrast coronary angio
2nd - non-invasive functional imaging
3rd - invasive coronary angiography
non-invasive functional
1. myocardial perfusion scintigraphy with SPECT)
- stress echo
- first-pass contrast-enhanced magnetic resonance (MR) perfusion or
- MR imaging for stress-induced wall motion abnormalities
