Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

A PACES > Cardio station > Flashcards

Cardio station Flashcards

1
Q

Why check for anaemia in aortic stenosis

A

Heydes syndrome

AS + Angiodysplasia

[also anaemia of chonic disease esp if elderly
-Very rare haemolysis through native valve ]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When is AS murmur loudest

A

held expiration
over aortic area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pulse in AS?

A

Slow rising / weak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Key thing to look for on exam if suspected AS?

A

Signs of cardiac decompensation
- Raised JVP
- Bibasal crackles
- Peripheral oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Key DDx of AS murmur

A

Systolic murmur
- Mitral regurg - should radiate to axilla
- HOCM
- Aortic sclerosis
- VSD especially if young
- Pulmonary stenosis - very rare and should be louder on inspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Ix AS

A

ECG - ?LVH / strain
Echo - confirm gradients and function
Bloods - Full blood count - anaemia / WCC
Inflam markers - CRP
Blood cultures ?IE
Chest xray ? overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Difference between murmur between AS and aortic sclerosis

A

Usually shorter and softer
Should not radiate to carotids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Aetiology of AS

A

80% degenerative calcific

congenital bicuspid valve

rare but possible - rheumatic fever and endocarditits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How to confirm severe aortic stenosis on exam? history? ix?

A

Exam
Nature of murmur - obliterates s2
slow rising pulse
evidence of cardiac decompensation

History
Angina and syncope

Ix
Echo
LVH on ECG / LBBB
[history of decompensation]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why ECG pre TAVI

A

10% go on to have PPM
?Pre existing conduction disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How to tell AS on echo

A

Peak gradient across valve >64
or mean gradient >40

[best measure is ratio of velocity over AV vs LVOT dimentional index]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When TAVI vs AVR

A

> 75 - likely TAVI

<75 - likely surgical - unless not fit

TAVI - more PPM, less bleeding risk
quicker recovery
less AF, Less CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Who is not suitable for a TAVI

A

Bad PVD
Malignant features of annulus
Bad CAD - would be too hard for stents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

in <75 Who might the surgeons not want to operate on for AVR

A

Previous chest radiotherapy
Previous sternotomy
patient LIMA to LAD
Pulm HTN
Severe LVSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Work up for a TAVI

A

Bloods - routine
Echo
ECG
If smoker - LFTs
Angio
TAVI CT
Consider carotid doppler

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Key complications of TAVI

A

PPM - 10%
Vascular issues - Fem artery
Stroke / coronary blockage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When is JVP classes as elevated

A

If >3cm above sternal notch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Life expectancy AS with decompensation

A

50% at 1 year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Murmurs louder when?

A

Right-sided murmurs
- Louder during inspiration.
- inspiration increases blood flow to the vena cava, which increases venous return to the right side of the heart.

Left-sided murmurs
- louder during expiration.
- expiration increases blood flow to the left side of the heart by constricting pulmonary vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is / When do you get paradoxical splitting of s2?
How to make it more obvious?

A

Paradoxical splitting of S2
This occurs when the pulmonary valve (P2) is heard before the aortic valve (A2).
This is caused by conditions like severe aortic stenosis or left bundle branch block.

During inspiration, paradoxical splitting causes narrow splitting of S2, and during expiration, it causes wide splitting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cardio exam

A

Hands
-Endocarditis / clubbing
- Brusing / bleeding - anticoagulated

Pulse
- AF, Radial-radial delay
- Any radial artery harvest
- collapsing pulse

Face
- Pallor
- corneal arcus

JVP

Back
-Lung bases
-sacral oedema

Chest
- Scar sternotomy
- Hickman scar
- PPM
- Audible click
- Palpation + apex

Auscultate
- include carotid
- turn to left side and bell for mitral valve

Failure
- Oedema
- Pulm odema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does a sternotomy scar mean

A

Valve replacement
CABG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Loud s2 but no sternmotomy scar

A

Pulm HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Ix in endocarditis

A

Full history and exam
Bedside obs esp pyrexia
ECG - cardiomyopathy / LVH
Urine dip - haematuria

Bloods
FBC CRP - infection / anaemia chronic disease
U&Es for end organ damage
LFTs prior to antibiotics
Coag / INR - if anticoagulated
Blood cultures x3

Imaging
CXR - failure
Echo +/- TOE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Mechanical vs bioprosthetic valves

A

Mechanical
- More durable - lasts life
- Lifelong WARFARIN only
(NOACs get thrombosis)

bio valve
- lasts 10-15 years
- Short duration anticoag post op

Endocarditis no difference between

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Syncope History

A

What do you mean?

What happened Before,
- Need to get the activity preceding
- Prev epsodes - any fainting

During
- Any witnesses
- Rigid?
- Tongue biting

After
- Recovery

Chest pain / haemoptysis

Drug history
-Any recent changes
- Hypertensives
- Drugs for arrhythmia

PMH
- Parkinsons - autonomic / postural
- Structural heart disease eg AS

Social history
- Roofers
- HGV / drive for work

Family history
- Sudden death / cardiomyopathy
- Anyone with collapses / devices in chest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Syncope vs seizure

A

Syncope - sudden onset
Cardiogenic - no prodrome
Quick recovery post

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Does presence of abnormal movements mean seizures?
Incontinence?
Tongue biting?

A

No common in syncope
- Usually fairly random and short lived
- Usually flaccid rather than rigid

Incontinence happens with all syncope

Tongue biting - particularly side and back of tongue - likely seizure
- Represents clonus of jaw

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Cardiac sounding syncope red flags

A

LOC without prodrome
Occurring on exertion
History of strucutal heart disease / family sudden death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Investigations in syncope

A

Pulse
Lying standing bp
Fingerprick glucose
12 lead ECG - structural / LVH / ectopy / QT interval / heart block / ion channel opathy

Bloods
HB - anaemia
WCC / CRP - infection
renal / liver - starting medications
Electrolytes / TFTs

Possible 24hr tape

Consider ECHO but not in first instance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are you looking for with 24 hr tape

A

Symptom rhythm correlation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

3 aspects of Management of vasovagal / neurogenic syncope

A

Patient education
- Avoid precipitants / triggers

Drink plenty of fluid
- Bolus water drinking

High sodium diet

Consider compression garments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Target blood pressure

A

<140/90 in clinic
<135/85 at home

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Hypertension history

A

How long

Secondary causes
RRTOPACCC
- Renal artery stenosis - tried ACEi
- Renal Ca - weight change
- Thyroid hyper
- OSA - daytime drowsiness
- Phaeo - hot flushes, palps,
chest pain, anxiety
- Cushings - steroids
- Carcinoid - flushing / diarrhoea
- Acromegaly - changes in appearance / hands
- Conns

End organ damage
- Kidney - frothy urine, kidney problems
- Brain - headaches, blurred vision, TIA / strokes, nose bleed
- Heart - chest pain, fluid overload, SOBOE

Social
- Liquorish - aldosterone effect
- Alcohol
- Ilicit drugs - cocaine
- Smoking

Meds
- Steroids for chronic conditions
- COCP
- Are they taking antihypertensives

PMH
- Surgery when young - coarctation
- Peripheral vascular disease
- Asthma / COPD / IBS - steroids -> cushings
- CKD

FamHx
- Family history
- High cholesterol
- Fam Hx RRT / CVA ?ADPCKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Hypertension investigations

A

Target organ damage
Kidneys
- Renal function - end organ damage and K+ for conns
- Renal dip for proteinuria + Albumin creatinine ratio
- Preg test
- If worried about renal artery stenosis need to do a CT
Heart
- ECG - LVH
- Consider Echo for LV mass
- CXR / BNP if any evidence of failure
Brain
- Imaging if headaches

Bloods
TFTs
HBa1c
Lipid profile
Consider - Aldolsterone renin ratio or dexamethasone supression test, pituitary profile

QRISK score

Ambulatory BP monitoring

Q RISK calculates a person’s risk of developing a heart attack or stroke over the next 10 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Hypertension exam

A

Check BP

Hands Radial-radial delay
Radial femoral delay

Perform fundoscopy
Look at back of neck for buffalo hump
Carotid / femoral bruis

Thyroid palpate

Abdo
Any striae - cuhings
Polycystic kidneys
Renal bruis

Urine Dip

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Simple things you might see on fundoscopy in HTN

A

AV nipping
flame haemorrhages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

HTN given ACE and then significant deterioration in renal function

A

Renal artery stenosis
- would expect a doubling in creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Conns Ix? what do you need to do prior

A

Aldosterone renin ratio

Need to stop antihypertensives that affect RASS
- Basically only one that doesnt is doxasosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Phaeo Ix? what affects this

A

Urinary / blood catecholamines
-Paracetamol on urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Cortisol excess test

A

Low dose dexamethasone suppression test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

OSA ix

A

sleep study looking at saturations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Raised aldosterone - what ix now

A

Renal vein sampling for aldosterone

CT scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Admit vs discharge hypertensive patient

A

Split into

Hypertensive urgency - sustained hypertension without end organ damage
- Aim to reduce diastolic pressure to <110
- Reduce MAP by no more than 25%

Hypertensive emergency - with end organ damage
- Aim to reduce diastolic to <115
-Use IV labetalol / GTN in a HDU environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Drug for phaeo emergency

A

Phentolamine
- alpha blocker

phaeo phento

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Acute pulm oedema secondary to hypertension management

A

IV labetalol + GTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Support to help patients with medication compliance

A

Education
Dossett box

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Hypertension treatment

A

Lifestyle
- Salt - especially bread
- Weight loss
- Excercise
- Alcohol and smoking

ACEi /ARB or CCB if >55 / Black
Both
Thiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Already on ACE / CCB / Thiazide
Next steps

A

Compliance issues

Add in spironolactone
B blockers/ Alpha blockers if tachy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Are HCM and HOCM the same

A

No - one is non obstructive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

how is HCM inherited ?

A

Autosomal dominant
- Most commonly (total 75%)

MYH7 gene - beta myosin heavy chain (MYosin Heavy)
MYBPC gene - Cardiac myosin binding protein C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

HCM exam findings

A

Young

Hands
-nil
- Pulse - AF most common arrhythmia / ectopics

Arms
-Nil

Neck
- Large a waves in JVP -

Chest
- Scars for myectomy / ICD (check sub cut in left axilla)
- Palpation left axilla, Heave, apex

Auscultate
- Often outflow murmur
- Mitral murmur
-Get patient do do Valsalva -> does it extenuate murmur

Heart failure
- Lung bases
- Pedal oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Young patient for cardio exam

A

HCM
Cardiomyopathy / channelopathy
Congenital heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Young person with syncope likely cardiac causes

A

Long QT
WPW
Brugada
HCM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What causes the a waves seen on JVP eg in HCM

A

forceful atrial contraction against non compliant RV
- due to septal hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What might the mitral murmur in HCM mean

A

Systolic anterior motion of the mitral valve
-> Mitral regurg

occurs when the anterior leaflet of the mitral valve moves toward the left ventricular outflow tract (LVOT) during systole which causes a LVOTO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Differentials of HCM if no device and systolic murmur in young person

A

Bicuspid aorta / aortic stenosis
VSD
Mitral valve disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Investigations HCM
What are you looking for?

A

12 lead ECG - rhythm / AF, large P waves if atrial enlargement
- narrow / broad QRS esp if fibrosis
- LVH - often with deep T waves in lateral leads

Bloods
- Consider genetic tests
[MYH7 gene - beta myosin heavy chain (MYosin Heavy)
MYBPC gene - Cardiac myosin binding protein C]
- Sometimes chronic low grade trop
- BNP if failure

CXR - Cardiomegaly

Echo
- LVH typically septum and asymmetric
- Systolic anterior motion of the mitral valve
- L atrial dilatation
- Measure gradient and consider exercise echo

CMRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Why MRI in HCM

A
  • Apical segment of HCM often not seen on echo
  • Can more accurately assess gradients
  • Can see scar - ectopic / ventricular arrhythmias focus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Management HCM

A

Cardio referral
Advise to notify DVLA especially if syncope / Ventricular arrhythmias / ICD

Conservative
- Clinical genetics + screening 1st degree relatives
- Cardiac imagining specialists
- Specialist nurses
- Aim to avoid dehydration
- Light exercise ok. Avoid weight lifting as can worsen outflow tract gradients

Medical
- Beta blockers / CCB - reduce outflow tract gradients.
- Be very careful using diuretics - especially if outflow tract obstruction

Surgical
- Primary prevention ICDs
- Septal myectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How to decide who gets ICD in HCM

A

Sudden death risk calculator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

HCM on BB what could you add

A

disapriamide - sodium channel blocker

Then either surgical or
- Mavacamten - Brand new - cardiac myosin inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Marfans looking patient what might you hear

A

Either / both
Mitral regurg
Aortic regurg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

where is the apex beat

A

5th intercostal space
Mid clavicular line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Polycythaemia diagnosis

A

Haematocrit >48% women and >49% in men

Must be persistently in that range

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Where precursor cell are red blood cells from? Other things this precursor can turn into?

A

Myeloid stem cells
- can become RBCs, platelets, and neutrophils, basophils, monocytes etc

[all white cells bar lymphocytes]

  • In polycythemia would expect changes in neuts and platelets
  • Lymphocytes should not be affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the types of polycythaemia

A

Apparent
- Due to eg dehydration

True
Primary = primary haem disorder polycythaemia ruba vera

Secondary (something making marrow produce more)

Appropriate
- Chronic lung disease
- Cyanotic disease
- OSA

Inappropriate - Exogenous epo
-testosterone
-PKD
-RCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Polycythaemia history

A

Why was the blood test done?
- Dehydration / alcohol / D&V

Hyper-viscosity symptoms
- Arterial / venous thrombosis
- Sometimes bleeding
- Head fog / headaches [think about waldenstroms if so]

PRV
- Sweats drenching
- Weight loss 10% / 6months
- Occationally fever
- Puritis after hot shower

Symptoms of splenomegaly
- Early satiety
- LUQ pain

Secondary causes
- Chronic lung issues
- Check for SOBOE
- Snoring Daytime solomence- OSA

-Known diagnosis of tumours

PMH
- Lung / heart disease

DH
- Any diuretics
- Testosterone

SH
- Smoking
- Alcohol

FH
-PKD or renal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Which conditions cause both arterial and venous thrombosis

A

Myeloproliferative disorders
- CML
- Essential thrombocythaemia
- Myelofibrosis

Antiphospholipid syndrome

Polycythaemia

Paroyxysmal nocturnal haemaglobinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Polycythaemia ruba vera test

A

JAK 2
- Also picks up 50% of essential thrombocythaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Polycythaemia investigations

A

Bedside
- Spo2
- Examine lung disease / organomegaly
- Evidence of thrombus

Bloods
- Repeat FBC
- Epo level and JAK 2

CXR
- Undiagnosed chronic lung disease

US abdo
- Renal tumours / PKD
- Splenomegaly

-Polysonography / sleep studies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Epo levels in primary vs secondary polycythaemia

A

Low in PRV

High in secondary causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Polycythaemia management

A

Referral to Haem

Conservative
- Stop smoking
- CV control
- Follow up as risk of developing AML

Medical
-Venesection Reduce haematocrit to 0.45 [If secondary depends on history of thrombosis and up to haem]
- Aspirin or clopi [Secondary don’t use]
- Treatment of thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

If patients cant tolerate venesection in polycythaemia, how else to reduce haematocrit? Risk?

A

Hydroxycarbamide

-> non selectivley reduces marrow production
-> can reduce all blood counts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

If struggling to differentiate MR and AS murmurs what other signs might help

A

MR may have AF and displaced apex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What would you expect to hear in AS? MR?

A

AS - crescendo decresecendo

MR - crescendo / pansystolic

71
Q

Differentiate mitral regur and tricuspid regurg murmurs

A

MR loudest expiration

TR - loudest inspiration

72
Q

When would you suspect VSD murmurs

A

Young - almost all are closed now
Very loud pansystolic most in inspiration

73
Q

Primary vs secondary MR

A

Primary
- Congential
- Degenerative- Mitral prolapse, age related
- Rheumatic heart disease
- Connective tissue disease

Secondary
- ischaemic heart disease
- heart failure
- Post endocarditis
- Ruptured cordae post MI
- Ilfiltrative

Functional
- LV dilation

74
Q

MR investigations

A

Bloods
FBC
U&E
BNP

ECG

Chest XR

Echo
Diagnosis and quantification
Mechanism
Also any other valves / haemodynamic issues such as LVD / atrial dilation

75
Q

Management of MR

A

Mild mod
Approx risk 5% of progression over 5 years
Need regular clinic review

Severe - anyone should be considered for intervention

[If severe and symptoms need intervention
Asymptomatic + AF / atrial dilation -> likely intervention
Asymptomatic and otherwise normal echo]

76
Q

What are the intervention options for MR and in who

A

Decisions made with surgeon, cardiologist and interventionist

Repair

Replace

Mitraclip
- those who open heart surgery would not be option
- through groin

77
Q

What are the clinical and echographic features of severe MR

A

Clinical
- AF
- thursting displaced apex beat (means LV dilation)
- palpable thrill

Echo
- measure MR jet
- evidence of LV dilation / impairment

78
Q
A
79
Q

Palps red flags?

Secondary causes

A

Syncope
Features heart failure

Previous cardiac history eg MI Scarring

Family history unexplained death

DH
Recent abx which prolong QT
Recreational drugs

Secondary
Phaeo
- Tremor weight loss htn sweating flusing
OSA - snoring weight / tiredness
Thyrotoxicosis

80
Q

Palps exam

A

Hands
Tremor
Pulse regular
BP eg phaeo

Face anaemia
Jvp / lung bases failure

Thyroid

Murmurs eg HCM
Valsava breath hold murmur

ICD scar look in axilla

Abdo flank mass

81
Q

Palps ix

A

Bloods + extended Electrolytes
TFTs
Consider BNP

CXR

ECG
Tape 24 vs 72 vs loop looking for rhythm symptom correlation

Echo - rule out structural heart disease
Rule in murmurs
- Ideally done prior to fleccanide

Occasionally CMRI

82
Q

What serious things are you looking to rule out on ecg Hx palps

A

Hcm - STE and t wave inversion

Brugada - Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave.

QT interval

ARVC - arrythmogenic right ventricular cardiomyopathy

(Brugada)

83
Q

What is ARVC arrythmogenic right ventricular cardiomyopathy?
Seen on ecg?

A

Autosomal dominant genetic disorder of myocardium in which there is fatty infiltration of the right ventricular free wall, predisposing to paroxysmal ventricular arrhythmias

  • second most common cause of sudden cardiac death

T wave inversion in right precordial leads V1-3, in absence of RBBB (85% of patients)
Epsilon wave (most specific finding, seen in 50% of patients)
Localised QRS widening in V1-3 (> 110ms)

84
Q

How to remember JVP waveforms
a,x,c,v,y

A

a - Atrial contraction
x - relaXation of atria
c- triCuspid Closure
v - Venous filling of atria
y - emptYing of atria

85
Q

Causes of dilated cardiomyopathy

A

ABCCCDD

Alcohol
Beri beri
Coxackie B virus
Cocaine
Chargras disease
Doxorubicin, Daunorubicin

86
Q

Name 3 of the named aortic regurg signs

A

Waterhammer pulse

Quicke’s sign: visible capillary pulsations in the fingernails
[caPINKY QUINKY]

De Musset’s sign: nodding of the head with each heartbeat
[Mullet head banging]

Becker’s sign: visible pulsations of retinal arteries and pupils

Muller’s sign: systolic pulsations of the uvula
[Muller Yoghurt]

Corrigan’s pulse: visible carotid pulsations
[corrigans carotid]

Rosenbach’s sign: systolic pulsations of the liver
Gerhard’s sign: systolic pulsations of the spleen

Traube’s sign: pistol shot femorals
Duroziez’s sign: ejection systolic and diastolic murmurs heard with the stethoscope when the bell is used to compress the femoral arteries

Hill’s sign: popliteal > brachial systolic pressure by > 60mmHg

87
Q

Spot diagnosis thinking aortic regurg might be the answer

A

Marfanoid body

88
Q

Aortic regurg exam

A

?Marfans

Hands
- IE

Feel both pulses

Collapsing pulse

Get BP

JVP / lung bases

Look in mouth at uvula - mullers sign
High arched palate

Parasternal heave + thrill

Auscultate
- Early diastolic murmur heard best over the LLSE with the patient leaned forward and in expiration
- Length of murmur correlates with severity (short is bad, volume of murmur is not)
- High-pitched, decrescendo murmur
- Ejection flow murmur over the aortic area (does not equate to co-existent aortic stenosis) from increased flow across the aortic valve

Legs - oedema

I would like a full set of observations especially BP and temperature. fundoscopy to assess for roth spots, Urine dip looking for blood

If time
- Palpate liver and spleen
- Rosenbach’s sign: systolic pulsations of the liver
Gerhard’s sign: systolic pulsations of the spleen
- Traube’s sign: pistol shot femorals
- Duroziez’s sign: ejection systolic and diastolic murmurs heard with the stethoscope when the bell is used to compress the femoral arteries

89
Q

AR murmur differentials

A

Austin-Flint murmur
- Functional mitral stenosis caused by regurgitant jet striking mitral valve leaflets
- Marker of severe AR
- Distinguished from MS in that there is no opening snap, S1 is not loud

PR / MS / TS very hard to hear

90
Q

On palpating pulse when does a systolic murmur come?

Diastolic

A

Systolic - just after pulse

Diastolic - just before pulse

91
Q

Causes of acute AR? Chronic? Signs on exam to find them?

A

Acute severe - Will have florid pulmonary oedema
- Acute aortic dissection
- Infective endocaritis - Fever, janeway, oslers
- Prosthetic valve failure eg trauma to chest

Chronic - D Bad CRRAMPSS
- Dilated arotic root
- Bicuspid valve
- Congentital
- Rheumatic heart disease
- Rheumatoid arthritis:
- Anklylosing spondylisis:
- Marfan’s syndrome: high, arched palate, long limbs
- Pseudoxanthoma elasticum: neck skin
- Syphilitic aortitis: Argyll-Robertson pupil (reacts to accommodation but not to light)
- Systemic lupus erythematosus:
rash, oral ulcers, alopecia

  • Hypertension / Calcific AV
  • Osteogenesis imperfecta: blue sclerae, hearing aids
92
Q

What are roth spots

A

Small, red spots with white or pale centers that appear on the retina of the eye.

They are caused by bleeding, or hemorrhages, and are usually round, oval, or flame-shaped.

Possibly in IE / Diabetes / hypertension / myeloma / leukaemia / HTN…

93
Q

What murmur

A

AR
Pseudoxanthoma elasticum

94
Q

Acute severe AR Investigations? Chronic?

A

Bedside
- Full set of obs especially BP and tempurature
- Urine dip for blood
- Fundoscopy for roth spots
- ECG - Evidence of LVH / strain eg TWI / LAD

Bloods
- Blood cultures
- Inflammatory markers
- NT ProBNP

CXR
Evidence of pulm pedema

Echo
- Vegitations / aortic root / look at central jet of AR / valve morphology

95
Q

Dilated aortic root on echo ->

A

Cardiac ct

96
Q

Management AR

A

Acute severe AR
- Referral to ICU for IV vasodilators + inotrope
- >Surgical valve replacement

Chronic
Patient education
- especially symptoms to look out for

Medical
- ACEi may provide symptomatic improvement
- If Marfanoid / Aortic root dilation - BB to reduce shear stress over valve

Surgical - If chronic AR + evidence of LVD or LVSD. OR if symptomatic
- If aortic root >55mm

97
Q

Transvalvular vs paravalvular regurg

A

Transvalvular - though middle of valve

Paravalvular - around valve, often a sign of dehiscnece

98
Q

What about AS murmur would make you think its severe

A

Long + Loss of second heart sound

99
Q

What scoring system for infective endocarditis? Major criteria?

A

Dukes
2 Major or 1 major and 3 minor

Major
- Typical blug in 2x BCs
- Echo findings

Minor
- Pyrexia
- suspicious echo
- embolic pneumonia
- prostehtic valve
- vasculitic crp/esr rise
- atypical organism in BCs

100
Q

Seen on ECG mitral stenosis

A

p mitrale - broad / bifid

AF

Right heart strain

101
Q

Cause of rheumatic fever? Criteria ? how to test for it? treatment?

A

Strep pyogenes
B haemolytic strep

Duckett-jones diagnostic criteria
[Throat swab
rapid antigen detection test
antistreptolysin O titre

+2 major criteria]

Rest, high dose aspirin and penicillin
-> long term penicillin prophylaxis

102
Q

Bar pansystolic loudest at apex what else might you describe in MR

A

Wide splitting of S2
Loudest on expiration

103
Q

Tricuspid regurg findings on exam

A

Raised JVP with large v waves
thrill left sternal edge
Pansystolic murmur loudest on inspiration
Reversed split left secodn heart sound

Pulsitile liver / ascities

Peripheral oedema

104
Q

Causes of tricuspid regurg

A

Either conditions causing RV failure
- functional - most common eg RV dilation eg post infarct
- Pulm HTN
- Rupture of papilary muscles

Conditions affecting Valve
- infective endocarditis
- rheumatic fever
- Congenitcal - ebsteins anomoly
- Marfans
- Libman sacks
- carcinoid

105
Q

Classic TR findings on ECG? CXR? Echo?

A

ECG - p-pulmonale (peaked p), RVH
CXR - Double right hear boarder (large RA)
Echo - TR, RV /RA dilation

106
Q

Pulmonary stenosis on exam

A

Raised JVP with giant A waves

L parasternal heave

ESM loudest on inspiration
Widely split second heart sound (delay in RV emptying)

RV failure - oedema / ascities …

107
Q

Severe PS murmur on auscultation

A

Loss of second heart sound

108
Q

ECG / CXR / Echo of PS

A

P Pulminale
RVH
RBBB

CXR - Oligaemic lung fields, Large RA / RV

Echo - Severity, RV function

109
Q

Congenital causes of PS

A

Tetralogy of fallot
- PS, RVH, VSD, Overriding aorta

Noonans
- think turners but in men

110
Q

Options for management of Pulm stenosis

A

Valvulotomy - if evidence of RV failure / raised gradient >70mmHg

Percutaneous pulm valve inplantation

Surgical repair / replace

111
Q

What common murmurs in normally functioning AVR ? MVR?

A

Flow murmur
in AVR - Systolic
- A diasolic AR murmur would indicate non funcitoning valve

MVR - Diastolic flow murmur normal
- MR would indicate non functioning valve

112
Q

Some non acute complications of surgical valves

A

Thromboembolus - 1% per year despite warfarin

Bleeding secondary to anticoagulation

Haemolysis - much more significant with old ball-in-cage valves and may be low grade with new Eg St Jude

Endocarditis

AF - especially MVR

Valve failure - especially if tissue (can get a valve-in-valve)
- May be calcification / dehiscence

113
Q

Indications for an ICD

A

Primary prevention
- MI > 4weeks ago +Severe LVSD + non-sustained VT in EP study / broad QRS
- Familal condition with high risk sudden caridac death
- LQTS, Brugada, HCM, Complex congenitcal heart disease

Secondary prevention
- Arrest due to VT / VF
- VT with haemodynamic compromise

CRT pacemakers consider if
- LVEF <35% NYHA >1 and on optimal medical therapy
- QRS >150ms

114
Q

Constrictive pericarditis signs on exam

A

Raised JVP

Prominent y descent (tricuspid opening)

Kussmals sign - increase in JVP on inspiration

Pulsus paradoxus - drop of >10mmHg on inspiration

Auscultation - pericardial knock

Ascities

Peripheral oedema

115
Q

Causes of constrictive pericarditis

A

TB - Cervical lymphadenopathy
Trauma / surgery
Tumour
Therapy (Radio)
connective Tissue disease - Rheum / SLE

TTTT

116
Q

Constrictive pericarditis investigations

A

CXR - calcification +/- TB
Echo - high signal from pericardium
CT - thickened pericardium
Cath - equalisaition of heart pressures

117
Q

Pathophysiology constrictive pericarditis

A

Thick fibrous capsule insulates heart from intrathroacic pressure changes with respiration
-> ventricular interdependence
- Filling one ventricle reduces size and filling of the other

118
Q

ASD murmur? what else on the exam might point towards this

A

Fixed splitting second heart sounds
- may have pulm ESM and diastolic tricuspid flow murmur

Downs syndrome

119
Q

2 types of ASD? Differentiate them on ECG

A

primum - AVSD (Downs)
- RBBB + LAD (wide bifid P)

Secundum - more common
- RBBB + RAD (Peaked p)

120
Q

Complications of ASD that you might find on exam

A

Irregular, tachycardic pulse – atrial tachyarrhythmias

Pronator drift – paradoxical emboli

Cyanosis, pulmonary hypertension, cor pulmonale – Eisenmenger’s syndrome

121
Q

ASD indications for closure?
Contraindication?

A

Symptomatic breathlessness
Paradoxical embolism
RV dilation
Significant shunt

Contraindication - Severe pulm HTN / Eisenmenger

122
Q

VSD murmur? Name 2 associations

A

Pansystolic - no audible S2

  • Tetralogy of fallot
  • turners
  • downs
  • PDA
  • Coarctation
123
Q

Surgical procedure that partially corrects fallots ? finding on exam?

A

Blalock - taussig shunt
- anastamose subclavian artery to pulm artery
- > Absent radial pulse

124
Q

Coarctation murmur ? what else on exam?

A

Continuous radiating to back
loud A2

  • Hypertension Right +/- L arm. lower in legs
  • Weak femoral pulses
125
Q

Coarctation associations

A

VSD
Turners
bicuspid aortic valve

126
Q

Coarctation seen on ECG / CXR

A

ECG - LVH, RBBB

CXR - rib notching, double aortic knuckle (due to post stenotic dilation)

127
Q

Coarctation management

A

Perc EVAR endovascular aortic repair
Surgical - patch aortoplasty

Follow up with angiograms (including cerebral for anneurysms.)

Long term antihypertensive management

128
Q

Patent ductus arteriosis - what is it?
key risk factor for developing during pregnancy?
Signs on exam?
2 key complications?
Management?

A

Aorta -> pulm artery connection with L->R shunt

Rubella

Collapsing pulse
thrusting apex
loud continuous murmur

Eisenmengers
Endocarditis

Perc / surgical closure

129
Q

If you suspect VSD in young person what should you comment on

A

Soft p2 - no evidence of pulm HTN

Apex not displaced, no overload, no Left parasternal heave suggesting RHF

130
Q

VSD in young patient differentials

A

ASD
PDA
MR
TR
Pulm stenosis
Tetralogy of fallot

131
Q

Tell me what you know about congenital heart disease

A

Can be differentiated into L->R and R->L shunts

L->R
- Associated with increased pulm blood flow
- Usually acyanotic
- May slowly lead to increased pulm, vascular resistance with pulm HTN and reversal of shunt called eisinmengers syndrome
- Eg VSD, ASD, AVSD, PDA

R->L
- Deoxygenated blood into aorta
- Tetralogy of fallot, Pulmonary atresia, transposition of great arteries, ebsteins abnormality, hypoplastic left heart syndrome

132
Q

Differentiate murmur of VSD and ASD / PDA

A

ASD
- usually just mid/ eject systolic and usually much softer
- Often has fixed splitting of the second heart sound
[Unlikely to get in paces]

PDA - continous murmur

133
Q

When might a VSD not be congenital

A

Post MI / trauma

134
Q

Who gets antibiotic prophlaxis in ACHD

A

Previous endocarditis
Eisinmengers syndrome
<6months since patch repair

135
Q

How are VSDs managed

A

Confirm diagnosis via echocardiography with assessment of shunting and pumonary pressures.

Small VSDs often managed with observation

any symptomatic/ endocarditis/large are repaired
- Patch
- Percutanous device closure

136
Q

eisenmenger syndrome management

A

Pulm vasodilators eg Sildenafil

Prophylactic Abx

Monitoring for hyperviscosity / secondary polycythaemia

Consider referral for heart-lung transplant

137
Q

How would you investigate this patinet who had clinical MR

A

Full history

Bedside
- ECG
- Observations esp pyrexia
- If acute consider inflam markers

Echocardiogram
- Severity of MR and cause

If consideration of surgery
- Would perform angiography toassess need for CABG at same time

138
Q

How can you tell severe MR clinically? Investigation?

A

Clinical
- Signs and symptoms of LVF
- Evidence of AF

Echo
- Usualy on colour flow doppler

139
Q

Heart sounds in MR

A

Pansystolic murmur which radiates to axilla

May get 3rd heart sound due to rapid LV filling

140
Q

Indications for surgery in MR

A
  • Evidence of LVSD / LV dilation
  • Symptomatic
141
Q

If you hear metalic first and second heart sound, especially if youngish what is most likely

A

Rheumatic heart disease

142
Q

Aetiology of valvular pathology
AS/AR/MR/MS

A

AS
- Degenerative calcific
- Bicuspid
- Rheumatic fever and endocarditis

AR
- Rheumatic heart disease
- Endocarditis
- Long standing HTN
- Connective tissue disease - Eg Ank Spond, Marfans, Osteogenesis inperfecta

MR
- Most common Functional caused by LV dilation
- Rheumatic heart disease
- degeneration
- Papilllary muscle rupture post MI
- Connective tissue eg Marfans / ehlers danlos

MS
- Almost always rheumatic heart disease (99%)
- Calcific valve disease / endocarditis

143
Q

Anaemia in metalic valve usually? other main causes?

A

Usually occult blood loss secondary to anticoag

Haemolysis - would have raised Bili

Sub acute endocarditis -> anaemia of chronic disease

144
Q

Which prostetic valve more likely to get clots?

A

MVR
-> lower velocities so clots can stick

145
Q

How would you work up a patient for valve replacement

A

Examination of the heart
- Detailed echo evaluation
- Angiogram - assess for CAD (simultaneous CABG)
- Carotid dopplers if AVR

Can the lungs handle it?
-Pulmonary function tests esp if smoker
- Anaesthetic assessment eg with CPET testing

Referral for MDT to discuss options eg Open vs perc / medical

146
Q

How would you manage prothetic valve endocarditis

A

MDT in hospital
Cardiology
ID / Micro
Cardiothoracic surgery

  • Highly likely to require surgery
  • Acute heart failure will require diruesis and W/H any heart failure meds
  • High dose IV antibiotics ideally post 3x blood cultures
147
Q

Hypertensive retinography grades

A
  1. subtle narrowing of arteries
  2. presence of AV nipping
  3. Infarction (cotton wool spots), and flame haemorrhages
  4. Swelling of optic disk - pappiloedema
148
Q

Name some causes of hypertension

A

Idiopathic essential (90%)

Renal - Eg Renal artery stenosis or PKD

Endocrine - Eg Cushing / conns

Anatomical - coarctation

Pre/Eclampsia

149
Q

How would you manage a hypertensive patient as OP

A

Lifestyle modifications
Esp Smoking cessation, Low salt, exercise, diabetic controll, reduced alcohol.

Check medication compliance
Baseline ECG looing for LVH
Check bloods especially FBC, TFTs and renal function prior to medication

Meds
ACE/CCB -> Thiazide + mineralocorticoid receptor antagonis

150
Q

Cardio Selective Beta blockers

A

Betaxolol
Acebutelol
Esmolol
Atenolol
Metoprolol

Mnemonic:
Betablockers Acting Exclusively At Myocardium

151
Q

Differeniate JVP and carotid pulse

A
  • JVP represents RA pressure
  • Can be seen between insertion points of sternocleidomastoid
  • JVP falls with inspiration and rises with expriation. Carotid does not
  • JVP can be increased with hepatojugular reflex
  • Not usually palpable
152
Q

Causes of a collapsing pulse

A

AR
PDA
AV fistula

153
Q

Findings in endocarditis

A

Non tender macular - Janeway lesions
Tender palpable - Olsers nodes
Spinter haemorrhages
Roth spots
Sternotomy scar
Murmurs
Cardiac failure

154
Q

Common organisms for infective endocarditis

A

Native valve
- Strep viridans
- staph aureus / Gram negative eg enterococcus
- Rare HAECK- Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, and Kingella species

Prosthetic
- Staph aureus or staph epidermis most common

155
Q

Cause of IE?

A

Any bacteraemia
Eg Infection of any sort
Injury to skin
Dental work

156
Q

Who is at risk of endocarditis

A

Anyone can get it
More likely in any valve abnormality / prothetic heart valves

157
Q

How does a vegetaition form

A

Damaged valve -> exposed endothelium
-> Thombus and bacteria attach

158
Q

Complications of IE

A

Heart failure - valve incompetence

Abscess in arotic root -> rhythm disturbance

Infective elboli
Eg brain, kidneys, bowel etc

159
Q

Indications for surgery in IE

A

-Large vegitations
-Severe AR / MR
-Heart failure
-Fungi

Prosthetic
-Evidence of dehiscnece
-Valve obstruction
-Abscess

Relapsing infection

160
Q

Bar bacterial what other types of endocarditis do you know?

A

Fungal

Libman-Sacks endocarditis (also known as murantic or verrucous endocarditis)
- nonbacterial endocarditis which involves the presence of sterile vegetations on the cardiac valves.
- Seen in SLE

Malignancy Eg pancreatic adenocarcinoma

161
Q

What are the causes of AF

A

Cardio
- IHD
- HTN
- Mitral valve disease
- cardiac surgery
- congenital heart disease
- pericarditis
- cardiomyopathy

Resp
- Infections
- Lung ca
- COPD
- PE
- Connective tissue disease

Abdo
- Alcoholic liver disease
- Any infection

Other
- Hyperthyroid

162
Q

2 main complications of AF

A

Strokes
Heart failure

163
Q

AF investigations

A

Bedside
A-E
ECG to confirm

Bloods
Inflam markers, renal function / Thyroid function, extended elctrolytes

CXR any heart failure
Echo - assess lv and and structural disease

164
Q

Tell me about some findings on examination of JVP ? Normal? pathological?

A

Marker of RA pressure with a normal rise and fall. Starts with A wave of atrial filling and ending with Y descent of atrial emptying

Specific findiings
- Raised - congested
- Prominent V waves and rasied - RV failure and tricuspid regurg
- Cannon A waves - Atrial contraction onto closed tricuspid in heart block
- Loss of A wave in AF as ineffective atrial contraction

165
Q

What is kussmals sign JVP

A

JVP raises in inspiration
- Should drop

Associated with severe heart failure of any cause
Suggests inability of RV to accept increasing volume of blood during inspired venous return

165
Q

How could you enhance murmur in MS

A

Squatting
Expiration

-> as increases cardiact output and flow

166
Q

What causes rheumatic fever

A

group A strep

166
Q

Rheumatic heart disease management

A

Ben pen
aspririn
Steroids

167
Q

Rheumatic fever criteria

A

Ducket jones criteria

168
Q

Mitral stenosis management

A

Heart failure management
AF management

Balloon valvulotomy
Surgical replacement

169
Q

Mitral stenosis complications

A

AF
Heart failure
Left atrial englargement -> dysphagia
Endocarditis

170
Q

Murmur in mitral prolapse

A

Systolic murmur with click as the posterior leaflet of the valve prolapses into Left atrium during systole

-> systolic click

171
Q

What are the causes of mitral valve prolapse? dd?

A

Click
- Congentital
- connective tissue eg marfans / elhers danlos
- Osteogenesis imperfecta
- pseudoxanthoma elasticum
- HCM
- PKD
- Rheumatic heart disease

Differentials
- Atrial myxoma
- Bicuspid aortic stenosis
- Endocarditis

172
Q

HFPEF evidence based treatment

A

SLG2 inhibitors
MRA eg spironolactone / eplenerone

173
Q

Causes of heart failure without LVSD

A

Right sided failure
Valvular lesions
HFPEF

174
Q

Why is this murmur TR rather than MR

A

Loudest on inspiration

Large v waves on JVP

Pulsitile liver

There is a history of IVDU and pyrexia

175
Q

What is a 3rd and 4th heart sound ? heard when?

A

S3 - rapid ventriuclar filling
- MR / TR / VSDs
- LV failure

s4 - tubulent blood flow into stiff ventricle
- Aortic stenosis, HTN, HCM, LVH

176
Q

How would you investigate / manage this patient with tricuspid regurg

A

Take a full history in particular asking about rheumatic fever history and recreational drug use

Bedside
ECG - RVH / arrythmias, Urine dip, fundoscopy, BP

Bloods
Blood culutes x 3 if suspicious of endocarditis
FBC and CRP for infection
U&Es as may need diuretics
Coag profile

Imaging
CXR - resp cause of TR eg pulm htn / cardiomegaly
Echo - endocarditis and heart falves / function

177
Q

Treatment of TR

A

Optomising cause eg connective tissue disease / lung function / endocarditis

Diruesis for symptoms

Surgical
may need valve replacement

178
Q

What is ebsteins abnomality

A

congenital defect in tricuspid valve position which causes tricuspid regug

Leads to atrialisation of a portion of the RV leading to an enlarged RA and a small RV

179
Q
A
180
Q

Asymptomatic Aortic stenosis when would you intervene

A

Inadequate BP response on treadmill
LV dysfunction

181
Q

Severe AS on echo

A

Gradient over 4m/s
Valve area < 1cm

A PACES (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions