Cardiology Flashcards

1
Q

stable angina investigation

A

coronary angiogram

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2
Q

treatment of stable angina

A

dual antiplatelet therapy

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3
Q

Investigation for a STEMI

A

already done an ECG so straight to angiogram as a troponin would take so long to come back

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4
Q

stable angina

A

ORBIT trial between PCI and medical therapy is on going.

stent if 70% stenosed with PCI

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5
Q

IHD investiation in stable

A

functional and anatomical

functional test for ischaemia like ETT
Anatomical Coronary angiogram

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6
Q

IHD ivx acute or unstable IHD

A

Serial ECG
Blood markers
Further tests

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7
Q

if no ST elevation and normal trop what could it be still and what would you do

A

unstable angina

aspirin/clopi/LMWH

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8
Q

no st elevation and raised trop

A

NSTEMI

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9
Q

IHD STABLE management catergories

A

Lifestyle
Medical Therapy
Revascularisation

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10
Q

Medical Therapy of STABLE IHD further categories

A

Preventative - antiplatelet
Symptoms - GTN spray, long acting nitrates
Alternative antianginals - BB

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11
Q

Types of revascualrisaiton of heart

A

PCI - baloons and stents

CABG

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12
Q

UNSTABLE IHD Mx

A

Pain - analgesia + oxygen
Ischaemia - aspirin and clopi plus antithrombotic treatment LMWH
Serial ECG

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13
Q

HF - Reduced ejection fraction is what type of failure

A

Systolic

HFrEF

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14
Q

Preserved ejection fraction is what type

A

HFpEF

diastolic failure

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15
Q

Chronic Heart Failure causes

A

Myocardial
Pressure
Arrhythmias

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16
Q

Myocardial causes of HF

A
IHD
Tocins
Infectious
INfiltrative
metabolic
genetic
17
Q

Pressure causes for HF

A
HTN
valvular disease
pericardial disease
high output
volume overload
18
Q

importance of diastolic heart failure

A

with something like AF where this no atrial contraction it relies on sucking from ventricles relaxing. This won’t happen! Need BB to slow AF?

19
Q

How IHD causes HF

A

Frank starling mechanism - increasing end diastolic pressure to try and increase output

hypertrophy from La Place relationship due to increase wall stress. More muscle fibre.

This hits a limit

then heart dilates

heart can’t maintain blood pressure with cardiac output so increasing Total preipheral resistance

salt and water retention to increase pre load.

RAAS - angiotenisin II to retain water and aldosterone release
Anit diuretic hormone from baroreceptors due to decreased BP

Adrenergic response to increase Peripheral vasculature through increased sympathetic tone of blood vessels

continuous sympathetic stimulation to increase HR - more cell death from ischaemia

eventually prelkoad is too much for heart - congested

the high levels of angiotensin/aldosterone increase cytokine production and get adverse heart remodelling

20
Q

signs of CHF

A
JVP
Hepatojugular reflux
Gallop
Displaced apex
Murmur