__Y6 Cardio Flashcards by Laura Tan

Causes of Aortic Regurg

Valvular - rheumatic, IE
Root - Connective tissues disease (Marfans)
Acute - post-aortic dissection

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Austin Flint Murmur

MDM - due to fluttering from MV following turbulant flow from aortic jet

Heard with AR

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Peripheral signs of AR

Quinke's (nailbed)
Corrigans (carotids)
De Mussets (head bobbing)
Mullers (uvula)
Traubes (pistol shot femorals)
Wide pulse pressure 
Collapsing pulse

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Marfan’s signs to demonstrate in exam

High arched palate
Arm span > height
Fingers around wrist (overlap)
Lax skin

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Taping apex beat (palpable first HS) heard with?

+ describe mechanism

Mitral stenosis

Increased LA pressure, holds MV out wider than normal
so slams shut slightly later and from a greater distance with increased force

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Loud S1
Opening snap
Mid-diastolic murmur

Mitral Stenosis

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Mitral Stenosis exam findings

Loud S1
Opening snap
Mid-diastolic murmur

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Common causes of AF

MI, valve disease, alcohol/caffeine, hyperthyroid

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What else other than AF can cause an irregularly irregular pulse?

And how to differentiate between them

Ventricular ectopics

Differentiate by exercising the patient
Ventricular ectopics will go away as they are not conducted when there is less diastolic filling time

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How do you know if AF is well controlled?

Pulse deficiet

Listen to heart and hear if everything is conducted down to radial pulse

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Complications of valve replacement

Early - early IC, increased bleeding/bruising, failure of valve

Late - late IE, failure/dysfunction, bleeding, thromboembolism, MAHA

Or use FIBAT mnemonic

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To complete examination of prosthetic valve pt?

EEE

Ensure INR checked (and HB for MAHA and bleeding)
Echo to check valve is working well
Endocarditis - advice about dental hygiene and red flags

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Stages of clubbing

FACE

Fluctuancy of nail bed
Angle loss
Curvature increased
Expansion

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Murmur loudest in aortic area, radiate to carotids, assoc features (BP narrow pulse pressure, slow rising carotid pulse)

Aortic stenosis

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Murmur loudest in apex, radiates to axilla, assoc features (displaced apex beat), pansystolic

Mitral regurg

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Murmur louder on inspiration, assoc features: elevated JVP, giant ‘v’ waves (earlobes), L parasternal heave, palpable liver

Tricuspid regurg

Murmur loudest in left lower sternal edge, when sitting forward, breath held in expiration, BP wide pulse pressure, collapsing pulse, displaced/heaving apex beat

Aortic regurgitation

irregularly irregular pulse, malar flush, tapping apex beat, left parasternal heave
Mid-diastolic murmur (after S2), opening snap

Mitral stenosis

Saddle-shaped ST elevation (‘concave) on ECG, pleuritic CP improves on sitting forwards

Acute pericarditis

Acute pericarditis ECG changes?

Saddle shaped ST elevation

Causes of acute pericarditis?

viral infection, TB, uraemia, trauma, post MI, CTD, hypothyroid

Signs of Infective Endocarditis

Hands - splinter haemorrhages, clubbing, petechiae
Chest - changing heart murmurs
Abdo - splenomegaly, microscopic haematuria

Other: fever, arthalgia, emboli, Roth spots, Janeway lesions, Osler’s nodes

Acute rheumatic fever major criteria

Duckett Jones Major criteria
(CASES)

Carditis
Arthritis
Subcutaneous nodules
Erythema marginatum
Sydenham's chorea

plus rising ASO/+ve throat culture for Strep A

Malar flush in cardio

Classically in mitral stenosis

Due to resulting CO2 retention and vasodilatory effects

Due to rapid venticular filling Early diastole during passive filling of compliant LV (can be normal) KEN-TUC-KY Seen with mitral regurg As atria overfilled with regurg so more rapid filling Also TR, VSD, post-MI, dilated CM

Caused by atria contracting forcefully to overcome an abnormally stiff ventricle (increased tubulent flow as atria contract) Late diastole during active filling of non-compliant LV TE-NESS-SEE Often heard in LVH, AS always abnormal

STEMI V1-V6

Anterior - LAD

STEMI II, III, aVF

Inferior - RCA

Describe three different types of HB

1st degree – all conducted with long PR 2nd degree – irregular QRS pattern, some conducted (type 1 ratio, type 2 changing PR) 3rd degree – none conducted, no association, totally regular QRS but not in association with P

STEMI management

ABCDE O2, Aspirin 300mg PO Nitrates/GTN Diamorphine IV 2.5mg-5mg Streptokinase 1.5 MU over 1 hour BB if not in HF ± Thrombolysis

ECG changes with PE

``` Sinus tachy RV strain (inverted T waves in V1-4) ``` Later - S1Q3T3

Displaced apex beat due to:

DILATATION not hypertrophy Dilatation due to volume overload (AR, MR, ASD/VSD) Concentric hypertrophy due to pressure overload (AS, HTN)

ECG changes in MI

1. ST elevation in first 4-12 hours 2. Pathologic Q waves (big) after 6 hours (indicate irreversible damage) 3. T wave inversion as ST normalise