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Finals > Cardiology > Flashcards

Cardiology Flashcards

1
Q

what is the MOA of ACEi

A

inhibits conversion of angiotensin 1 to II - causes vasodilation and reduced blood pressure // reduces stimulation for aldosterone release decreasing socium and water retention by the kidneys

ACEi - dilate efferent arterioles, reduce glomerular capillary pressure

monitor urea and electrolytes before treatment is initiated and after increasing the dose

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2
Q

side effects and contra-indications of ACE inhibitors

A

cough
angioedema
hyperkalaemia
first-dose hypotension

C/I
pregnancy and breastfeeding
renovascular disease
aortic stenosis - may cause hypotension
patients with high dose diuretic therapy

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3
Q

causes of acute pericarditis

A

viral infections (Coxsackie)
tuberculosis
uraemia
post-myocardial infarction
early (1-3 days): fibrinous pericarditis
late (weeks to months): autoimmune pericarditis (Dressler’s syndrome)
radiotherapy
connective tissue disease
systemic lupus erythematosus
rheumatoid arthritis
hypothyroidism
malignancy
lung cancer
breast cancer
trauma

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4
Q

features of acute pericarditis

A

inflammation of pericardial sac for <4-6w

chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include a non-productive cough, dyspnoea and flu-like symptoms
pericardial rub

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5
Q

what are some findings in acute pericarditis

A

ECG changes
PR depression
global/widespread saddle-shaped ST elevation

transthoracic echocardiography

bloods
inflammatory markers
troponin: around 30% of patients may have an elevated troponin - this indicates possible myopericarditis

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6
Q

management of acute pericarditis

A

IPT mx if high risk features - fever >38, elevated troponin

otherwise OPT
treat underlying cause
avoid strenuous activity until sx resolution
1st line - NSAIDs and colchicine

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7
Q

indications for adenosine

A

termination of supraventricular tachycardia by causing transient heart block in AVN

effects enhanced by dipuridamole (antiplatelet) and blocked by theophyllines

adverse effects: chest pain, bronchospasm, transient flushing

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8
Q

adult ALS - non-shockable rhythms

A

non-shockable rhythms - asystole, PEA

adrenaline 1mg ASAP

repeat adrenaline 1mg every 3-5mins

chest compressins 30:2

give thrombolysis if PE suspected

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9
Q

adult ALS - shockable rhythms

A

VF/pulseless VT

chest compressions 30:2

single shock + 2 mins CPR
(if cardiac arrest witnessed - 3 stacked shocks then CPR)

adrenaline 1mg after 3 shocks, repeat 3-5min

amiodarone 300mg after 3 shocks, amiodarone 150mg after 5 shocks (lidocaine if unavailable)

give thrombolysis if PE suspected

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10
Q

reversible causes of cardiac arrest

A

Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia

Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade – cardiac
Toxins

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11
Q

when to use amiodarone

A

amiodarone is class III antiarrhythmic agent to treat atrial, nodal and ventricular tachycardias

give into central veins
may cause arrhythmia due to prolongation of QT interval

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12
Q

adverse effects of amiodarone

A

thyroid dysfunction: both hypothyroidism and hyper-thyroidism
corneal deposits
pulmonary fibrosis/pneumonitis
liver fibrosis/hepatitis
peripheral neuropathy, myopathy
photosensitivity
‘slate-grey’ appearance
thrombophlebitis and injection site reactions
bradycardia
lengths QT interval

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13
Q

drug management of angina pectoris

A

aspirin and statin
sublingual glyceryl trinitrate to abort angina attacks

beta-blocker or CCB
if CCB monotherapy - use rate limiting (verapamil, diltiazem)

+ both

+ 3rd drug whilst patient is awaiting assessment for PCI or CABG

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14
Q

when to use antiplatelets

A

ACS - lifelong aspirin, 12month ticagrelor

PCI - lifelong aspirin and 12m prasugrel/ticagrelor

TIA - lifelong clopidogrel

ischaemic stroke - lifelong clopidogrel

peripheral arterial disease - lifelong clopidogrel

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15
Q

what are the features of aortic dissection

A

tear in the tunica intima of the wall of the aorta

features:
sharp tearing chest/back pain
pulse deficit - weak/absent carotid, brachial, or femoral pulse
aortic regurgitation
hypertension

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16
Q

what is aortic dissection associated with

A

hypertension: the most important risk factor
trauma
bicuspid aortic valve
collagens: Marfan’s syndrome, Ehlers-Danlos syndrome
Turner’s and Noonan’s syndrome
pregnancy
syphilis

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17
Q

classifications of aortic dissection

A

Stanford classification
type A - ascending aorta, 2/3 of cases
type B - descending aorta, distal to left subclavian origin, 1/3 of cases

DeBakey classification
type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
type II - originates in and is confined to the ascending aorta
type III - originates in descending aorta, rarely extends proximally but will extend distally

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18
Q

investigation of aortic dissection

A

Chest x-ray
widened mediastinum

CT angiography CAP - for stable patients and for planning surgery
false lumen = aortic dissection

Transoesophageal echocardiography (TOE)
more suitable for unstable patients who are too risky to take to CT scanner

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19
Q

management of aortic dissection

A

Type A
surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention

Type B*
conservative management
bed rest
reduce blood pressure IV labetalol to prevent progression

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20
Q

chronic causes of aortic regurgitation

A

due to valve disease:

rheumatic fever: the most common cause in the developing world

calcific valve disease

connective tissue diseases e.g. rheumatoid arthritis/SLE

bicuspid aortic valve (affects both the valves and the aortic root)

aortic root disease:
bicuspid aortic valve (affects both the valves and the aortic root)

spondylarthropathies (e.g. ankylosing spondylitis)

hypertension
syphilis
Marfan’s, Ehler-Danlos syndrome

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21
Q

acute causes of aortic regurgitation

A

infective endocarditis
aortic dissection

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22
Q

features of aortic regurgiation

A

early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
collapsing pulse
wide pulse pressure
Quincke’s sign (nailbed pulsation)
De Musset’s sign (head bobbing)
mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams

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23
Q

how is aortic regurgitation managed

A

medical management of any associated heart failure
surgery: aortic valve indications include
symptomatic patients with severe AR
asymptomatic patients with severe AR who have LV systolic dysfunction

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24
Q

clinical features of aortic stenosis

A

chest pain
dyspnoea
syncope / presyncope (e.g. exertional dizziness)
murmur
an ejection systolic murmur (ESM) is classically seen in aortic stenosis
classically radiates to the carotids
this is decreased following the Valsalva manoeuvre

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24
Q

features of severe aortic stenosis

A

narrow pulse pressure
slow rising pulse
delayed ESM
soft/absent S2
S4
thrill
duration of murmur
left ventricular hypertrophy or failure

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25
Q

causes of aortic stenosis

A

degenerative calcification (most common cause in older patients > 65 years)
bicuspid aortic valve (most common cause in younger patients < 65 years)
William’s syndrome (supravalvular aortic stenosis)
post-rheumatic disease
subvalvular: HOCM

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26
Q

managing aortic stenosis

A

asymtpomatic - observe
symptomatic - valve replacement
asymptomatic but valvular gradient >40 - consider surgery

options for AVR
surgical AVR is the treatment of choice for young, low/medium operative risk patients
transcatheter AVR (TAVR) is used for patients with a high operative risk
balloon valvuloplasty - used in children with no aortic valve calcification

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27
Q

what is arrhythmogenic right ventricular cardiomyopathy

A

inherited CVD presenting with syncope or sudden cardiac death (2nd after HOCM)

AD inheritance, right ventricular myocardium replaced by fatty and fibrofatty tissue

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28
Q

features of arrhythmogenic right ventricular cardiomyopathy

A

presents with palpitations, syncope, and sudden cardiac death

ECG abnormalities in V1-3, T wave inversion
50% pt have an episilon wave (terminal notch)
echo - enlarged hypokinetic right ventricle with thin free wall

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29
Q

management of arrhythmogenic right ventricular cardiomyopathy

A

drugs - sotalol
catheter ablation - prevent ventricular tachycardia
implantable cardioverter defibrillator

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30
Q

definition and types of atrial fibrillation

A

most common sustained cardiac arrhythmia

first detected episode - irrespective of symptomatic or self-terminating

recurrent episodes - >2 episodes
if terminates spontaneously - paroxysmal AF (episodes last <7 days)
if non-self terminating - persistent AF

permanent AF - continuous AF cannot be cardioverted

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31
Q

features of atrial fibrillation

A

Symptoms
palpitations
dyspnoea
chest pain

Signs
an irregularly irregular pulse

ECG - absent p waves and irregularly irregular QRS complexes

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32
Q

rate management of atrial fibrillation

A

beta blocker or a rate limiting calcium channel blocker (diltiazem)

offer if <48h, start rate control if >48h

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33
Q

rhythm management of atrial fibrillation

A

offer if onset <48h

e.g., digoxin
risk of stroke when restored to sinus rhythm - therefore need to have short sx duration <48h or be anticoagulated for a period of time before attempting cardioversion

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34
Q

how to use the CHA2DS2-VASc score

A

congestive heart failure
hypertension
age >75
diabetes
prior stroke, TIA or thromboembolism
vascular disease disease
sex

score 0 - no treatment
score 1 - consider anticoagulation
score 2 - offer anticoagulation

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35
Q

anticoagulation in AF

A

assess need for anticoagulation - CHADs2 VASc

assess bleeding risk - ORBIT score

DOACs
apixaban
dabigatran
edoxaban
rivaroxaban

warfarin - second line

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36
Q

how is cardioversion used in atrial fibrillation

A

emergency electrical cardioversion when pt is haemodynamically unstable

elective electrical/pharmacological cardioversion when rhythm control strategy is preferred

if AF <48h - heparinise
cardiovert using electrical DC cardioversion or amiodarone

if AF >48h - 3w anticoagulation prior to cardioversion then 4w anticoagulation

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37
Q

what drugs are used in pharmacological cardioversion

A

amiodarone
flecainide - if no structural heart disease

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38
Q

treatment of AF post-stroke

A

long term stroke prevention - warfarin or direct thrombin inhibitor or fXa inhibitor (apixaban)

start anticoag immediately after TIA
start after 2w if acute stroke, with antiplatelet therapy in interim

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39
Q

when is catheter ablation used in AF

A

used when poor response to antiarrhythmic medication

anticoagulate 4 weeks before and during procedure

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40
Q

what is atrial flutter + ECG findings

A

supraventricular tachycardia - rapid atrial depolarisation waves

ECG - sawtooth appearance
atrial rate 300/min
ventricular (HR) based on degree of AV block - e.g., 2:1 block = 150/min ventricular rate

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41
Q

how is atrial flutter managed

A

managed similar to AF (medication may be less effective)
more sensitive to cardioversion
radiofrequency ablation of tricuspid valve isthmus - curative

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42
Q

features of atrial myxoma

A

most common primary cardiac tumour, occurs in left atrium and in F

Features
systemic: dyspnoea, fatigue, weight loss, pyrexia of unknown origin, clubbing
emboli
atrial fibrillation
mid-diastolic murmur, ‘tumour plop’
echo: pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum

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43
Q

what are the recognised atrial septal defects and their features

A

ASF - most likely congenital heart defect in adulthood

Features
ejection systolic murmur, fixed splitting of S2
embolism may pass from venous system to left side of heart causing a stroke

ostium secundum (70% ASDs)
assx Holt Oram syndrome (tri-phalangeal thumbs)
ECG: RBBB with RAD

ostium primum
presents earlier
abnormal AV valves
ECG: RBBB with LAD, prolonged PR interval

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44
Q

what are the types of atriventricular block

A

AV block = impaired electrical conduction between atria and ventricular

1st degree heart block - PR >0.2s

2nd degree heart block - type 1 - prolongation of PR interval until dropped beat
type 2 - PR constant but P wave not often followed by QRS

third degree - complete
no association between P waves and QRS

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45
Q

what is B-type natriuretic peptide

A

BNP - hormone produced mainly by left ventricular myocardium in response to strain that causes vasodilation, diuretic and natriuretic, suppresses SNS and RAAS

raised levels may be caused by - reduced excretion in CKS, myocardial ischaemia, valvular disease

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46
Q

what are the uses of BNP

A

diagnosing patients with acute dyspnoea

ruling out heart failure

prognosis in chronic heart failure

guiding treatment in chronic heart failure

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47
Q

some indications for beta blockers

A

angina
post-myocardial infarction
heart failure: beta-blockers were previously avoided in heart failure but there is now strong evidence that certain beta-blockers improve both symptoms and mortality
arrhythmias: beta-blockers have now replaced digoxin as the rate-control drug of choice in atrial fibrillation
hypertension: the role of beta-blockers has diminished in recent years due to a lack of evidence in terms of reducing stroke and myocardial infarction.
thyrotoxicosis
migraine prophylaxis
anxiety

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48
Q

some side effects of beta blockers

A

bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction

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49
Q

contra-indications for beta-blockers

A

uncontrolled heart failure
asthma
sick sinus syndrome
concurrent verapamil use: may precipitate severe bradycardia

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50
Q

uses of direct thrombin inhibitors

A

Bivalirudin is a reversible direct thrombin inhibitor used as an anticoagulant in the management of acute coronary syndrome.

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50
Q

features of broad complex tachycardias

A

ventricular tachycardias

Features suggesting VT rather than SVT with aberrant conduction
AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 ms

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51
Q

what is brugada syndrome

A

autosomal dominant CVS disease causing sudden cardiac death

managed with implantable cardioverter defibrillator

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52
Q

what are the ECG changes seen in brugada syndrome

A

partial RBBB
convex ST elevation V1-V3 followed by negative T wave

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53
Q

what are the features of buerger’s disease (thromboangiitis obliterans)

A

small and medium vessel vasculitis assx with smoking

Features
extremity ischaemia
intermittent claudication
ischaemic ulcers
superficial thrombophlebitis
Raynaud’s phenomenon

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54
Q

normal oxygen saturation levels seen in cardiac catheterisation

A

IVC/SVC - 70%
RA, RV, PA - 70%

lungs oxygenate blood to 98-100% - LA, LV should saturate 98-100%

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55
Q

what are the time frames for cardiac enzymes

A

myoglobin - rises 1-2h, peaks 6-8h

CK - 4-8h, peaks 16-24h

trop T - rises 4-6h, peaks 12-24h

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56
Q

what are the differences between troponin I and T

A

troponin I - unique to heart muscle

troponin T - troponin T exists in other types of muscle

troponin levels increase 3-12h after heart attack

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57
Q

features of cardiac tamponade

A

cardiac tamponade - accumulation of pericardial fluid under pressure

Beck’s triad:
hypotension
raised JVP
muffled heart sounds

dyspnoea
tachycardia
an absent Y descent on the JVP - this is due to the limited right ventricular filling
pulsus paradoxus - an abnormally large drop in BP during inspiration
Kussmaul’s sign - much debate about this
ECG: electrical alternans

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58
Q

management for cardiac tamponade

A

urgent pericardiocentesis

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59
Q

features of hypertrophic obstructive cardiomyopathy

A

Leading cause of sudden cardiac death in young athletes

Usually due to a mutation in the gene encoding β-myosin heavy chain protein

Common cause of sudden death

Echo findings include MR, systolic anterior motion (SAM) of the anterior mitral valve and asymmetric septal hypertrophy

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60
Q

causes of dilated cardiomyopathy

A

Classic causes include
alcohol
Coxsackie B virus
wet beri beri
doxorubicin

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61
Q

causes of restrictive cardiomyopathy

A

Classic causes include
amyloidosis
post-radiotherapy
Loeffler’s endocarditis

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62
Q

types of acquired cardiomyopathy

A

peripartum cardiomyopathy
typical develops between last month of pregnancy and 5 months post-partum
More common in older women, greater parity and multiple gestations

takotsubo cardiomyopathy
‘Stress’-induced cardiomyopathy e.g. patient just found out family member dies then develops chest pain and features of heart failure
Transient, apical ballooning of the myocardium
Treatment is supportive

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63
Q

causes of chest pain

A

aortic dissection
pulmonary embolism
myocardial infarction
perforated peptic ulcer
boerhaaves syndrome

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64
Q

drug therapy guidelines for chronic heart failure

A

1 - ACEi, beta-blocker

2 - aldosterone antagonist

SGLT-2 inhibitors

3 - ivabradine, sacubitril valsartan, digoxin, hydralazine, cardiac resynchronisation therapy

offer annual influenza vaccine
one off pneumococcal vaccine

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65
Q

NYHA classification of chronic heart failure

A

NYHA Class I
no symptoms
no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations

NYHA Class II
mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea

NYHA Class III
moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

NYHA Class IV
severe symptoms
unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

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66
Q

features of coarctation of aorta

A

infancy: heart failure
adult: hypertension
radio-femoral delay
mid systolic murmur, maximal over the back
apical click from the aortic valve
notching of the inferior border of the ribs (due to collateral vessels) is not seen in young childre

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67
Q

features of complete heart block

A

heart failure
regular bradycardia (30-50 bpm)
wide pulse pressure
JVP: cannon waves in neck
variable intensity of S1

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68
Q

causes and features of constrictive pericarditis

A

causes - any cause of pericarditis, TB

dyspnoea
right heart failure: elevated JVP, ascites, oedema, hepatomegaly
JVP shows prominent x and y descent
pericardial knock - loud S3
Kussmaul’s sign is positive

CXR - pericardial calcification

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69
Q

hypertension management in diabetes mellitus

A

DM patients need strict BP control to reduce overall cardiovascular risk

BP targets for intervention should be 135/85 mmHg or 130/80mmHg if albuminuria or >2 features of metabolic

ACEi or A2RBs - regardless of age

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70
Q

causes of dilated cardiomyopathy

A

most common form of cardiomyopathy

idiopathic: the most common cause
myocarditis: e.g. Coxsackie B, HIV, diphtheria, Chagas disease
ischaemic heart disease
peripartum
hypertension
iatrogenic: e.g. doxorubicin
substance abuse: e.g. alcohol, cocaine
inherited: either a familial genetic predisposition to DCM or a specific syndrome e.g. Duchenne muscular dystrophy
around a third of patients with DCM are thought to have a genetic predisposition
a large number of heterogeneous defects have been identified
the majority of defects are inherited in an autosomal dominant fashion although other patterns of inheritance are seen
infiltrative e.g. haemochromatosis, sarcoidosis

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71
Q

features of dilated cardiomyopathy

A

classic findings of heart failure
systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
S3
‘balloon’ appearance of the heart on the chest x-ray

dilated heart leading to predominately systolic dysfunction
all 4 chambers are dilated, but the left ventricle more so than right ventricle
eccentric hypertrophy (sarcomeres added in series) is seen

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72
Q

specific rules for CVS disorders RE DVLA

A

hypertension - can drive unless unacceptable S/E

CABG - 4 weeks off

ACS - 4 weeks off

angina - driving must cease if sx occur at rest

pacemaker - 1 week off

implantable cardioverter defibrillator - for ventricular arrhythmia cease driving for 6m, prophylactically implanted, cease driving for 1m

aortic aneurysm - notify DVLA

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73
Q

ECG: atrial and ventricular hypertrophy signs

A

LVH - S wave (V1) + R wave (V5/V6) exceeds 40mm

RVH

LA enlargement - bifid p wave lead II >120ms

RA enlargement - tall p waves in lead II and V1

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74
Q

causes of left axis deviation

A

left anterior hemiblock
left bundle branch block
inferior myocardial infarction
Wolff-Parkinson-White syndrome* - right-sided accessory pathway
hyperkalaemia
congenital: ostium primum ASD, tricuspid atresia
minor LAD in obese people

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75
Q

causes of right axis deviation

A

right ventricular hypertrophy
left posterior hemiblock
lateral myocardial infarction
chronic lung disease → cor pulmonale
pulmonary embolism
ostium secundum ASD
Wolff-Parkinson-White syndrome* - left-sided accessory pathway
normal in infant < 1 years old
minor RAD in tall people

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76
Q

bi-fascicular block vs trifascicular block on ECG

A

bi-fascicular block - RBBB with LAD

trifascicular block - bifascicular block + 1st degree HB

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77
Q

coronary territories on ECG

A

anteroseptal - V1-V4
inferior - II, III, aVF
anterolateral - V1-6, I, aVL
lateral - I, aVL, V5, V6
posterior - changes in V1-3, reciprocal changes of STEMI

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78
Q

ECG signs of digoxin toxicity

A

down-sloping ST depression (‘reverse tick’, ‘scooped out’)
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia

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79
Q

ECG features of hypokalaemia

A

U waves
small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT

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80
Q

ECG features of hypothermia

A

bradycardia
‘J’ wave (Osborne waves) - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias

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81
Q

LBBB and RBBB on ECG

A

MaRRoW
in LBBB there is a ‘W’ in V1 and a ‘M’ in V6
in RBBB there is a ‘M’ in V1 and a ‘W’ in V6

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82
Q

ECG changes on acute myocardial infarction

A

hyperacute T waves - for a few minutes
ST elevation
T waves become inverted <24 hours - lasting days - months
pathological Q waves develop after several hours to days

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83
Q

ECG definition of STEMI

A

clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
1.5 mm ST elevation in V2-3 in women
1 mm ST elevation in other leads
new LBBB (LBBB should be considered new unless there is evidence otherwise)

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84
Q

some normal variants in ECG

A

sinus bradycardia
junctional rhythm
first degree heart block
Mobitz type 1 (Wenckebach phenomenon)

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85
Q

causes of a prolonged PR interval on ECG

A

idiopathic
ischaemic heart disease
digoxin toxicity
hypokalaemia*
rheumatic fever
aortic root pathology e.g. abscess secondary to endocarditis
Lyme disease
sarcoidosis
myotonic dystrophy

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86
Q

causes of ST depression on ECG

A

secondary to abnormal QRS (LVH, LBBB, RBBB)
ischaemia
digoxin
hypokalaemia
syndrome X

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87
Q

causes of ST elevation on ECG

A

myocardial infarction
pericarditis/myocarditis
normal variant - ‘high take-off’
left ventricular aneurysm
Prinzmetal’s angina (coronary artery spasm)
Takotsubo cardiomyopathy
rare: subarachnoid haemorrhage

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88
Q

causes of inverted T waves

A

myocardial ischaemia
digoxin toxicity
subarachnoid haemorrhage
arrhythmogenic right ventricular cardiomyopathy
pulmonary embolism (‘S1Q3T3’)
Brugada syndrome

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89
Q

what is wellen’s syndrome

A

ECG pattern caused by high-grade stenosis in LAD coronary artery

ECG features
biphasic or deep T wave inversion in V2-3
minimal ST elevation
no Q waves

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90
Q

what is eisenmenger’s syndrome

A

reversal of left to right shunt in congenital heart defect due to pulmonary hypertension

uncorrected shunt leads to remodelling of pulmonary microvasculature, causes obstruction to pulmonary blood and pulmonary hypertension

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91
Q

features of eisenmenger’s syndrome

A

Features
original murmur may disappear
cyanosis
clubbing
right ventricular failure
haemoptysis, embolism

associations - ventricular septal defect, atrial septal defect, patent ductus arteriosus

managed by heart-lung transplantation

92
Q

definition of acute heart failure

A

sudden onset or worsening of the symptoms of heart failure

AHF without a past history of heart failure is called de-novo AHF. Decompensated AHF is more common (66-75%) and presents with a background history of HF.

93
Q

causes of de-novo heart failure

A

caused by increased cardiac filling pressures and myocardial dysfunction usually as a result of ischaemia

Causes reduced cardiac output and therefore hypoperfusion - can cause pulmonary oedema.

less common causes of de-novo AHF are:
Viral myopathy
Toxins
Valve dysfunction

94
Q

causes of decompensated heart failure

A

Acute coronary syndrome
Hypertensive crisis
Acute arrhythmia
Valvular disease

There is generally a history of pre-existing cardiomyopathy. It usually presents with signs of fluid congestion, weight gain, orthopnoea and breathlessness.

95
Q

classification of heart failure symptoms

A

With or without hypoperfusion
With or without fluid congestion

96
Q

signs and symptoms of acute heart failure

A

symptoms - breathlessness, reduced exercise tolerance, oedema, fatigue

signs - cyanosis, tachycardia, elevated JVP, displaced apex beat, chest signs (bibasal crackles but may also cause wheeze), S3 heart sound

97
Q

investigations for patients with acute heart failure

A

bloods - any underlying abnormalities (anaemia, abnormality, abnormality electrolytes, infection)

chest x-ray - pulmonary venous congestion, interstitial oedema, cardiomegaly

echo - for new onset HF and for patients with known HF with change in heart function

BNP - raised levels indicate myocardial damage

98
Q

features of chronic heart failure

A

dyspnoea
cough: may be worse at night and associated with pink/frothy sputum
orthopnoea
paroxysmal nocturnal dyspnoea
wheeze (‘cardiac wheeze’)
weight loss (‘cardiac cachexia’): occurs in up to 15% of patients. Remember this may be hidden by weight gained secondary to oedema
bibasal crackles on examination
signs of right-sided heart failure: raised JVP, ankle oedema and hepatomegaly

99
Q

acute management of heart failure

A

recommended for all patients - IV loop diuretics (furosemide)

additional treatments - oxygen (94-98%), vasodilators

if respiratory failure - CPAP

if hypotensive - inotropic agents, vasopressor agents, mechanical criculatory assistance
opiates

100
Q

what are the types of heart failure classification

A

by ejection fraction
by time
by left/right
by high/low output

101
Q

types of ejection fraction issues in heart failure

A

reduced LVEF - <35-40% - HF-rEF
preserved LVEF - HF-pEF

systolic dysfunction
Ischaemic heart disease
Dilated cardiomyopathy
Myocarditis
Arrhythmias

diastolic dysfunction
Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis

102
Q

left sided heart failure

A

typically develops left sided heart failure due to increased left ventricular afterload (arterial hypertension or aortic stenosis) or increased left ventricular preload (aortic regurgitation resulting in backflow to the left ventricle)

left ventricular failure results in:
pulmonary oedema
dyspnoea
orthopnoea
paroxysmal nocturnal dyspnoea
bibasal fine crackles

103
Q

right sided heart failure

A

Right-sided heart failure is caused by either increased right ventricular afterload (e.g. pulmonary hypertension) or increased right ventricular preload (e.g. tricuspid regurgitation).

Right ventricular failure typically results in:
peripheral oedema
ankle/sacral oedema
raised jugular venous pressure
hepatomegaly
weight gain due to fluid retention
anorexia (‘cardiac cachexia’)

104
Q

high-output heart failure

A

high output heart failure refers to a situation where a ‘normal’ heart is unable to pump enough blood to meet the metabolic needs of the body.

Causes
anaemia
arteriovenous malformation
Paget’s disease
Pregnancy
thyrotoxicosis
thiamine deficiency (wet Beri-Beri)

105
Q

what are the heart sounds

A

S1 - closure of mitral and

S2 - closure of aortic and pulmonary valves
soft in aortic stenosis

S3 - diastolic filling of ventricle
heard in left ventricular failure, constrictive pericarditis

S4 - heard in aortic stenosis, HOCM, HTN, caused by atrial contraction against a stiff ventricle

106
Q

causes of loud S1

A

mitral stenosis
left-to-right shunts
short PR interval, atrial premature beats
hyperdynamic states

107
Q

causes of quiet S1

A

mitral regurgitation

108
Q

causes of loud S2

A

hypertension: systemic (loud A2) or pulmonary (loud P2)
hyperdynamic states
atrial septal defect without pulmonary hypertension

109
Q

causes of soft S2

A

aortic stenosis

110
Q

Causes of fixed split S2

A

atrial septal defect

111
Q

Causes of a widely split S2

A

deep inspiration
RBBB
pulmonary stenosis
severe mitral regurgitation

112
Q

features of hypercalcaemia

A

‘bones, stones, groans and psychic moans’
corneal calcification
shortened QT interval on ECG
hypertension

113
Q

types of xanthoma seen in hyperlipidaemia

A

Palmar xanthoma
remnant hyperlipidaemia
may less commonly be seen in familial hypercholesterolaemia

Eruptive xanthoma are due to high triglyceride levels and present as multiple red/yellow vesicles on the extensor surfaces (e.g. elbows, knees)
(caused by familial hypertriglyceridaemia, lipoprotein lipase deficiency)

Tendon xanthoma, tuberous xanthoma, xanthelasma
(caused by familial hypercholesterolaemia, remnant hyperlipidaemia)

114
Q

what are xanthelasma

A

Xanthelasma are yellowish papules and plaques caused by localized accumulation of lipid deposits commonly seen on the eyelid. They are also seen in patients without lipid abnormalities.

115
Q

definition of hypertension

A

a clinic reading persistently above >= 140/90 mmHg, or:
a 24 hour blood pressure average reading >= 135/85 mmHg

116
Q

causes of hypertension

A

primary (essential)
secondary - secondary to endocrine, renal, other causes

  • Glomerulonephritis
  • Chronic pyelonephritis
  • Adult polycystic kidney disease
  • Renal artery stenosis
  • Primary hyperaldosteronism
  • Phaeochromocytoma
  • Cushing’s syndrome
  • Liddle’s syndrome
  • Congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
  • Acromegaly
  • Glucocorticoids
  • NSAIDs
  • Pregnancy
  • Coarctation of the aorta
  • Combined oral contraceptive pill
117
Q

symptoms and screening of HTN

A

if severely raised: headaches
visual disturbance
seizures

check for end organ damage
fundoscopy: to check for hypertensive retinopathy
urine dipstick: to check for renal disease, either as a cause or consequence of hypertension
ECG: to check for left ventricular hypertrophy or ischaemic heart disease

118
Q

diagnosis and testing in hypertension

A

24 hour blood pressure

urea and electrolytes: check for renal disease, either as a cause or consequence of hypertension
HbA1c: check for co-existing diabetes mellitus, another important risk factor for cardiovascular disease
lipids: check for hyperlipidaemia, again another important risk factor for cardiovascular disease
ECG
urine dipstick

119
Q

management of hypertension

A

ACEi - first line if <55, avoid if pregnant, check renal function after starting

CCB - first line if >55y or AC pt

Thiazide type diuretics

A2RB - used if ACEi are not tolerated

120
Q

stages of hypertension

A

Stage 1 hypertension Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg

Stage 2 hypertension Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg

Severe hypertension Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg

121
Q

managing high readings

A

If the difference in readings between arms is more than 20 mmHg then the measurements should be repeated.

take a second reading during the consultation, if the first reading is > 140/90 mmHg

offer ABPM or HBPM to any patient with a blood pressure >= 140/90 mmHg.

If the blood pressure is >= 180/120 mmHg refer to specialists if signs of organ damage or life-threatening symptoms, phaeo?, and request urgent ix for end organ damage

122
Q

how is ambulatory BP monitoring used

A

Ambulatory blood pressure monitoring (ABPM)
at least 2 measurements per hour during the person’s usual waking hours (for example, between 08:00 and 22:00)
use the average value of at least 14 measurements

ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension)
treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 10% or greater

ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension)
offer drug treatment regardless of age

123
Q

features of hypertrophic obstructive cardiomyopathy

A

autosomal dominant disorder of muscle tissue due to defective contractile proteins - causes death in young

causes diastolic dysfunction: LVH -> poor compliance, reduced CO

often asymptomatic
exertional dyspnoea
angina
syncope following exercise (subaortic hypertrophy of the ventricular septum results in functional aortic stenosis)
sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure
jerky pulse, large ‘a’ waves, double apex beat
systolic murmurs

124
Q

echo findings in HOCM

A

MR SAM ASH
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)

125
Q

ECG findings in HOCM

A

left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
atrial fibrillation may occasionally be seen

126
Q

management of HOCM

A

Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*

127
Q

definition and cause of hypothermia

A

Mild hypothermia: 32-35°C
Moderate or severe hypothermia: < 32°C

Exposure to cold in the environment is the major cause
Inadequate insulation in the operating room
Cardiopulmonary bypass
Newborn babies.

Risk factors:
General anaesthesia
Substance abuse
Hypothyroidism
Impaired mental status
Homelessness
Extremes of age

128
Q

signs of hypothermia

A

shivering
cold and pale skin. Frostbite occurs when the skin and subcutaneous tissue freeze, causing damage to cells.
slurred speech
tachypnoea, tachycardia and hypertension (if mild)
respiratory depression, bradycardia and hypothermia (if moderate)
confusion/ impaired mental state

129
Q

how to investigate hypothermia

A

Temperature

12 lead ECG - acute ST-elevation and J waves or Osborn waves may appear

FBC, serum electrolytes. Haemoglobin and haematocrit can be elevated (due to haemoconcentration)

Blood glucose

Arterial blood gas
Coagulation factors
Chest X-ray

130
Q

managing hypothermia

A

Initial management includes:
Removing the patient from the cold environment and removing any wet/cold clothing,
Warming the body with blankets
Securing the airway and monitoring breathing,
If the patient is not responding well to passive warming, you may consider maintaining circulation using warm IV fluids or applying forced warm air directly to the patient’s body
+ rapid re-warming can lead to peripheral vasodilation and shock

131
Q

risk factors for infective endocarditis

A

previous episode of endocarditis

if prev normal valves - affects mitral valve

rheumatic valve disease (30%)
prosthetic valves
congenital heart defects
intravenous drug users (IVDUs) - will cause tricuspid lesion

132
Q

causative organisms for infective endocarditis

A

staphylococcus aureus - most common cause, common in acute presentation and IVDU

streptococcus viridans - poor dental hygiene

staphylococcus epidermidis (coagulase negative) - indwelling lines, post-surgery

133
Q

major and minor criteria in modified duke criteria

A

diagnosis of infective endocarditis if:
pathological criteria positive // 2 major criteria // 1 major and 3 minor criteria // 5 minor criteria

major - positive blood cultures, persistent bacteraemia, positive serology, evidence of endocardial involvement

minor - previous heart condition, microbial evidence, >38C, vascular phenomena, immunological phenomena

134
Q

management of infective endocarditis

A

initial therapy
amoxicillin (+gent) if native valve
if C/I, MRSA or sepsis - vancomycin + gent
vancomycin + rifampicin + gent if prosthetic valve

if native + staph - flucloxicillin
prosthetic + staph - flucloxacillin + rifampicin + gent

if strep - benzylpenicillin

if penallergic - vanc + gent

135
Q

investigations indicated in patient with palpitations

A

12 lead ECG
TFTs
U+Es
FBC

Holter monitoring - continuously records ECG from 2-3 leads for 24h

136
Q

what is isolated systolic hypertension

A

common in elderly - treat with same stepwise fashion as standard HTN

137
Q

what is ivabradine

A

Ivabradine is a class of anti-anginal drug which works by reducing the heart rate. It acts on the If (‘funny’) ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity.

Adverse effects
visual effects, particular luminous phenomena, are common
headache
bradycardia, heart block

138
Q

what are the JVP waves

A

a wave - atrial contraction
cannon a wave - atrial contraction against closed tricuspid

c wave - closure of tricuspid

v wave - passive filling in atrium against closed tricuspid

y descent - opening of tricuspid

139
Q

what is long QT syndrome

A

delayed repolarization of the ventricles, may lead to ventricular tachycardia/torsade de pointes, can cause sudden death

140
Q

causes of long QT

A

congenital

drugs
amiodarone, sotalol, class 1a antiarrhythmic drugs
TCAs, SSRIs, erythromycin, haloperidolm ondansetron

other
hypocalcaemia/kalaemia/magnesaemia
acute MI
myocarditis
hypothermia
SAH

141
Q

use of loop diuretics and examples

A

Furosemide and bumetanide - inhibit the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl

indication:
heart failure: both acute (usually intravenously) and chronic (usually orally)
resistant hypertension, particularly in patients with renal impairment

142
Q

features of mitral regurgitation

A

occurs when blood leaks back through the mitral valve on systole
can cause the myocardium to thicken over time -> fatigue and heart failure

usually asymptomatic
may have left ventricle failure symptoms

pansystolic blowing murmur, loudest at apex, radiates into axilla

143
Q

causes of mitral regurgitation

A

post MI
mitral valve prolapse
infective endocarditis
rheumatic fever
congenital

144
Q

treatment of mitral regurgitation

A

acutely, nitrates, diuretics, positive inotropes - to increase CO

if HF - ACEi and BB and spironolactone

if severe - surgery

145
Q

features of mitral stenosis

A

obstruction of blood flow across the mitral valve from the left atrium to the left ventricle - leads to increases in pressure within the left atrium, pulmonary vasculature and right side of the heart.

dyspnoea, haemoptysis

mid-late diastolic murmur
loud SI
opening snap
malar flush

146
Q

management of mitral stenosis

A

if assx with AF - anticoagulation with warfarin or DOAC

if asymptomatic - regular echo

if symptomatic - percutaneous mitral balloon valvotomy, mitral valve surgery

147
Q

features of mitral valve prolapse

A

atypical chest pain or palpitations

mid-systolic click (occurs later if patient squatting)

late systolic murmur (longer if patient standing)

complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death

148
Q

features and causes of ejection systolic murmur

A

if louder on expiration - aortic stenosis, hypertrophic obstructive cardiomyopathy

if louder on inspiration - pulmonary stenosis,
atrial septal defect

also: tetralogy of Fallot

149
Q

features and causes of pansystolic murmur

A

mitral/tricuspid regurgitation (high-pitched and ‘blowing’ in character)

tricuspid regurgitation becomes louder during inspiration, unlike mitral reguritation
during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole
ventricular septal defect (‘harsh’ in character)

150
Q

features and causes of late systolic murmur

A

mitral valve prolapse
coarctation of aorta

151
Q

features and causes of early diastolic murmur

A

aortic regurgitation (high-pitched and ‘blowing’ in character)

Graham-Steel murmur (pulmonary regurgitation, again high-pitched and ‘blowing’ in character)

152
Q

features and causes of mid-late diastolic murmur

A

mitral stenosis (‘rumbling’ in character)

Austin-Flint murmur (severe aortic regurgitation, again is ‘rumbling’ in character)

153
Q
A
154
Q

what is RILE

A

Right-sided murmur → heard best on Inspiration

Left-sided murmur → heard best on Expiration

155
Q

some complications of MI

A

cardiac arrest
cardiogenic shock
chronic heart failure
tachyarrhythmias
bradyarrhythmias
pericarditis
left ventricular aneurysm
left ventricular free wall rupture
ventricular septal defect
acute mitral regurgitation

156
Q

drugs used in the secondary prevention of MI

A

dual antiplatelet therapy (aspirin plus a second antiplatelet agent - ticagrelor and prasugrel)
ACE inhibitor
beta-blocker
statin

if acute MI and sx of heart failure or LV systolic dysfunction, treat with aldosterone antagonist post MI

157
Q

acute management of a STEMI

A

aspirin 300mg

ticagrelor or prasugrel (if PCI)

unfractionated heparin (if PCI)

PCI - gold standard

if no access to PCI <2h - thrombolysis with tissue plasminogen activator (-plase)
ECG 90mins after thrombolysis to assess if 50% resolution - if not, rescue PCI

158
Q

causes of myocarditis

A

viral: coxsackie B, HIV
bacteria: diphtheria, clostridia
spirochaetes: Lyme disease
protozoa: Chagas’ disease, toxoplasmosis
autoimmune
drugs: doxorubicin

159
Q

presentation and features of myocarditis

A

inflammation of the myocardium

Presentation
usually young patient with an acute history
chest pain
dyspnoea
arrhythmias

bloods - inflammatory markers++, cardiac enzymes++, BNP++

ECG - tachycardia, arrhythmia, ST/T wave changes

160
Q

management of myocarditis

A

treat underlying cause
supportive treatment

161
Q

uses and effects of nicorandil

A

vasodilatory drug used to treat angina

potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.

dverse effects
headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration

162
Q

uses and effects of nitrates

A

vasodilators used in angina and acute mx of HF

nitrates cause the release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels
in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand

Side-effects
hypotension
tachycardia
headaches
flushing

163
Q

features and causes of orthostatic hypotension

A

Orthostatic hypotension is more common in older people and patients who have neurodegenerative disease (e.g. Parkinson’s) diabetes, or hypertension

Iatrogenic causes include alpha-blockers (e.g. for benign prostatic hyperplasia).

Features
a drop in BP (usually >20/10 mm Hg) within three minutes of standing
presyncope
syncope

164
Q

managing orthostatic hypotension

A

treatment options include midodrine and fludrocortisone

165
Q

indications for temporary pacemaker

A

symptomatic/haemodynamically unstable bradycardia, not responding to atropine
post-ANTERIOR MI: type 2 or complete heart block
post-INFERIOR MI complete heart block is common and can be managed conservatively if asymptomatic and haemodynamically stable
trifascicular block prior to surgery

166
Q

indications and examples of parenteral anticoagulation

A

used for the prevention of venous thromboembolism and in the management of acute coronary syndrome

unfractionated heparin
LMWH

fondaparinux SC - activates antithrombin III, inhibits coagulation factors Xa

direct thrombin inhibitors - bivalirudin IV

167
Q

adverse signs in peri-arrest bradycardia (requiring treatment)

A

shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
syncope
myocardial ischaemia
heart failure

168
Q

treatment of peri-arrest bradycardia

A

atropine 500mcg IV (up to maximum 3mg)

transcutaneous pacing

isoprenaline/adrenaline infusion

there is potential risk of asystole

169
Q

adverse signs in peri-arrest tachycardia (requiring treatment)

A

shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
syncope
myocardial ischaemia
heart failure

170
Q

treatment of peri-arrest tachycardia

A

synchronised DC shocks - up to 3 then expert help

broad complex - assume ventricular, give loading dose amiodarone then 24h infusion
broad irregular - seek expert help

narrow complex - vagal manouvres, IV adenosine
narrow irregular - ?AF, consider chemical cardioversion or BB

171
Q

causes and definition of postural hypotension

A

Postural hypotension may be defined as a fall of systolic blood pressure > 20 mmHg on standing.

Causes
hypovolaemia
autonomic dysfunction: diabetes, Parkinson’s
drugs: diuretics, antihypertensives, L-dopa, phenothiazines, antidepressants, sedatives
alcohol

172
Q

features of premature ventricular complexes/beats

A

beats originating in the ventricular myocardium - common, idiopathic (may be due to HTN or MI)

usually asymptomatic
palpitations, irregular pulse

ECG - wide QRS

173
Q

management of patients with biological valves

A

will structurally deteriorate and calcify over time - given to pt >65y

warfarin for 3m
long term low dose aspirin

174
Q

management of patients with mechanical valves

A

low failure rate
increased risk of thrombosis - long term warfarin and low dose aspirin

target INR - aortic (3), mitral (3.5)

175
Q

significance of pulmonary artery occlusion pressure monitoring

A

indirect measure of left atrial pressure and filling pressure of left heart

normal - 8-12mmHg

176
Q

features of pulmonary embolism

A

chest pain
typically pleuritic
dyspnoea
haemoptysis
tachycardia
tachypnoea
respiratory examination

The relative frequency of common clinical signs is shown below:
Tachypnea (respiratory rate >16/min) - 96%
Crackles - 58%
Tachycardia (heart rate >100/min) - 44%
Fever (temperature >37.8°C) - 43%

177
Q

what is the PERC

A

used to exclude PE in patients with low pre-test probability

age >50
HR >100
O2 <94
prev DVT/PE
recent surgery <4w
haemoptysis
unilateral leg swelling
oestrogen use

if all absent, PE probability <2%

178
Q

when to use 2 level PE wells score (and features)

A

when PE is suspected

Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
An alternative diagnosis is less likely than PE 3
Heart rate > 100 beats per minute 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1
Malignancy (on treatment, treated in the last 6 months, or palliative)

179
Q

how to interpret a wells score

A

if PE likely (>4 pt) - CTPA, therapeutic anticoagulation until scan performed
if CTPA negative consider proximal leg vein USS

if PE unlikely - d dimer, if + do CTPA, if - consider alternative diagnosis

180
Q

when to use CTPA vs VQ scan

A

CTPA preferred

VQ if renal impairment as no need for contrast

181
Q

investigation findings in PE

A

d dimer - high sensitivity, low specificity - +++

ECG - S1Q3T3, RBBB, sinus tachycardia

CXR - usually normal, may have wedge-shaped opacification

CTPA - peripheral emboli may be missed

VQ scan - mismatch

182
Q

drugs used in managing VTE

A

DOAC - apixaban, rivaroxaban once diagnosis suspected, continue if dx confirmed

if DOAC is C/I
LMWH then dabigatran/edoxaban

severe renal impairment - LMWH, unfractionated heparin

if haemodynamically unstable - thrombolysis

183
Q

duration of anticoagulation therapy in VTE

A

ALL 3m

if provoked - stop after 3m
if cancer - stop after 3-6m
if unprovoked - 6m

184
Q

meaning of pulsus paradoxus + causes

A

greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration

severe asthma, cardiac tamponade

185
Q

meaning of slow rising pulse + causes

A

Slow-rising/plateau
aortic stenosis

186
Q

meaning of collapsing pulse + causes

A

aortic regurgitation
patent ductus arteriosus
hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)

187
Q

meaning of pulsus alternans + causes

A

regular alternation of the force of the arterial pulse
severe LVF

188
Q

meaning of bisferiens pulse + causes

A

‘double pulse’ - two systolic peaks
mixed aortic valve disease

189
Q

meaning of jerky pulse + causes

A

hypertrophic obstructive cardiomyopathy*

190
Q

causes and diagnosis of rheumatic fever

A

develops following an immunological reaction to a recent (2-4 weeks ago) Streptococcus pyogenes infection

Diagnosis is based on evidence of recent streptococcal infection accompanied by:
2 major criteria
1 major with 2 minor criteria

191
Q

criteria for diagnosing rheumatic fever

A

Evidence of recent streptococcal infection
raised or rising streptococci antibodies,
positive throat swab
positive rapid group A streptococcal antigen test

major criteria
erythema marginatum
Sydenham’s chorea
polyarthritis
carditis and valvulitis (eg, pancarditis)
subcut nodules

Minor criteria
raised ESR or CRP
pyrexia
arthralgia (not if arthritis a major criteria)
prolonged PR interval

192
Q

management of rheumatic fever

A

antibiotics: oral penicillin V
anti-inflammatories: NSAIDs are first-line
treatment of any complications that develop e.g. heart failure

193
Q

adverse effects of statins

A

myopathy
liver impairment - check LFT at baseline, 3m, 12m

194
Q

contraindications to statin therapy

A

macrolides - stop statin until pt completes course of ABx
pregnancy

195
Q

indications for statin therapy

A

all pt with established CVS risk
anyone with 10 year CVS risk >10%
T1DM pt diagnosed >10years ago or >40y or established nephropathy

196
Q

doses of statins for prevention of CVS disease

A

atorvastatin 20mg - primary prevention
atorvastatin 80mg for secondary prevention

197
Q

what are the characteristics and definition of an SVT

A

sudden onset narrow complex tachycardia
usually AVNRT, AVRT, junctional tachy

198
Q

management and prevention of supraventricular tachycardias

A

vagal manouvres - valsalva, carotid sinus massage

IV adenosine - rapid bolus 6mg -> 12mg -> 18mg
(C/I in asthmatics)

electrical cardioversion

prevention - beta-blockers
radiofrequency ablation

199
Q

definition and main causes of syncope

A

a transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery

reflex
orthostatic
cardiac

200
Q

causes of reflex syncope

A

vasovagal: triggered by emotion, pain or stress. Often referred to as ‘fainting’
situational: cough, micturition, gastrointestinal
carotid sinus syncope

most common in all age groups

201
Q

causes of orthostatic syncope

A

primary autonomic failure: Parkinson’s disease, Lewy body dementia
secondary autonomic failure: e.g. Diabetic neuropathy, amyloidosis, uraemia
drug-induced: diuretics, alcohol, vasodilators
volume depletion: haemorrhage, diarrhoea

202
Q

causes of cardiac syncope

A

arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular)
structural: valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy
others: pulmonary embolism

203
Q

how to investigate a patietn with syncope

A

cardiovascular examination
postural blood pressure readings: a symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg is considered diagnostic
ECG for all patients
other tests depend on clinical features
patients with typical features, no postural drop and a normal ECG do not require further investigations

204
Q

features and management of syndrome X

A

angina-like chest pain on exertion
ST depression on exercise stress test
but normal coronary arteries on angiography

nitrates

205
Q

definition and features of takayasu’s arteritis

A

large vessel vasculitis causing occlusion of aorta, causing absent limb pulse

most common in younger females and asians

features
systemic features of a vasculitis e.g. malaise, headache
unequal blood pressure in the upper limbs
carotid bruit and tenderness
absent or weak peripheral pulses
upper and lower limb claudication on exertion
aortic regurgitation (around 20%)

205
Q

investigations and management of takayasu’s arteritis

A

Investigations
vascular imaging of the arterial tree is required to make a diagnosis of Takayasu’s arteritis
either magnetic resonance angiography (MRA) or CT angiography (CTA)

Management
steroids

206
Q

definition and features of takotsubo cardiomyopathy

A

non-ischaemic cardiomyopathy associated with a transient, apical ballooning of the myocardium, may be triggered by stress

chest pain
features of heart failure
ECG: ST-elevation
normal coronary angiogram

supportive treatment

207
Q

moa and adverse effecs of thiazide diuretics

A

inhibit sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter - causes K+ loss

prev used in HTN but now replaced by thiazide- like diuretics e.g., indapamide

S/E
dehydration
postural hypotension
hypokalaemia
hyponatraemia
hypercalcaemia

208
Q

action of thrombolytic drugs

A

thrombolytic drugs activate plasminogen to form plasmin - degrades fibrin, breaks down thrombi - used in STEMI, acute ischaemic stroke, PE

examples - alteplase, tenecteplase, streptoinase

209
Q

contraindications to thrombolysis

A

active internal bleeding
recent haemorrhage, trauma or surgery (including dental extraction)
coagulation and bleeding disorders
intracranial neoplasm
stroke < 3 months
aortic dissection
recent head injury
severe hypertension

210
Q

definition and causes of torsades de pointes

A

form of polymorphic ventricular tachycardia associated with a long QT interval - deteriorates into VF, leads to sudden death

causes
congenital
antiarhythmics
tricyclic antidepressants
antipsychotics
chloroquine
terfenadine
erythromycin

211
Q

management of torsades de pointes

A

IV magnesium sulphate

212
Q

signs of tricuspid regurgitation

A

pan-systolic murmur
prominent/giant V waves in JVP
pulsatile hepatomegaly
left parasternal heave

213
Q

causes of tricuspid regurgitation

A

right ventricular infarction
pulmonary hypertension e.g. COPD
rheumatic heart disease
infective endocarditis (especially intravenous drug users)
Ebstein’s anomaly
carcinoid syndrome

214
Q

steps of the valsalva manouvre

A
  1. Increased intrathoracic pressure
  2. Resultant increase in venous and right atrial pressure reduces venous return
  3. The reduced preload leads to a fall in the cardiac output (Frank-Starling mechanism)
  4. When the pressure is released there is a further slight fall in cardiac output due to increased aortic volume
  5. Return of normal cardiac output
215
Q

causes of ventricular septal defect

A

most common cause of congenital heart disease - close spontaneously in around 50% of cases.

congenital VSDs are often association with chromosomal disorders
(Down’s syndrome, Edward’s syndrome, Patau syndrome, cri-du-chat syndrome)
congenital infections
acquired causes - post-myocardial infarction

216
Q

management of ventricular septal defects

A

small, asymptomatic VSF - close spontaneously, need monitoring

moderate - large - cause HF in few months - give medication of HF (diuretics), surgical closure of defect

may cause eisenmenger’s, RHF, pulmonary HTN

217
Q

types of ventricular tachycardia

A

monomorphic VT: most commonly caused by myocardial infarction

polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval

218
Q

management of ventricular tachycardia

A

f the patient has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure) then immediate cardioversion is indicated

amiodarone: ideally administered through a central line
lidocaine: use with caution in severe left ventricular impairment
procainamide

Verapamil should NOT be used in VT

219
Q

moa of warfarin

A

inhibits epoxide reductase preventing the reduction of vitamin K to its active hydroquinone form
this in turn acts as a cofactor in the carboxylation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.

220
Q

indications for warfarin

A

mechanical heart valves - INR 3 for aortic, 3.5 for mitral

used second line to DOAC - VTE INR 2.5, recurrent VTE 3.5, AF INR 2.5

221
Q

factors potentiating warfarin

A

liver disease
P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin
cranberry juice
drugs which displace warfarin from plasma albumin, e.g. NSAIDs
inhibit platelet function: NSAIDs

222
Q

p450 inducers

A

antiepileptics: phenytoin, carbamazepine
barbiturates: phenobarbitone
rifampicin
St John’s Wort
chronic alcohol intake
griseofulvin
smoking (affects CYP1A2, reason why smokers require more aminophylline)

223
Q

p450 inhibitors

A

antibiotics: ciprofloxacin, clarithromycine/erythromycin
isoniazid
cimetidine,omeprazole
amiodarone
allopurinol
imidazoles: ketoconazole, fluconazole
SSRIs: fluoxetine, sertraline
ritonavir
sodium valproate
acute alcohol intake
quinupristin

224
Q

management guidelines for high INR

A

major bleeding - stop warfarin, IV VK 5mg, prothrombin complex concentrate

INR >8 + minor bleeding - stop warfarin, IV VK 1-3mg, restart warfarin when INR <5

INR >8 no bleeding - stop warfarin, vitamin K 1-5mg, restart when INR <5

INR 5-8 minor bleeding - stop warfarin, IV VK 1-3mg, restart when INR <5

INR 5-8 no bleeding - withhold 1-2 doses, reduce subsequent maintenance dose

225
Q

features of wolff-parkinson white

A

due to a congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT)

the accessory pathway does not slow conduction so AF can degenerate rapidly to VF

226
Q

ECG features of WPW

A

short PR interval
wide QRS complexes with a slurred upstroke - ‘delta wave’
left axis deviation if right-sided accessory pathway
right axis deviation if left-sided accessory pathway

227
Q

treatment of wolff parkinson white

A

definitive treatment: radiofrequency ablation of the accessory pathway
medical therapy: sotalol, amiodarone, flecainide

Finals (27 decks)

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