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Cardiology Flashcards

1
Q

State the arterial supply to the lateral leads

A

Circumflex

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2
Q

Name the leads that correlate to the lateral area of the heart

A

I
aVL
V5
V6

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3
Q

State the arterial supply to the inferior leads

A

right coronary artery

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4
Q

State the arterial supply to the anteroseptal leads

A

LAD

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5
Q

Name the leads that correlate to the inferior area of the heart

A

II
III
aVF

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6
Q

Name the leads that correlate to the anteroseptal area of the heart

A

VI
V2
V3
V4

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7
Q

What is the initial management of ACS?

A 
o2 if <94%
12 lead ECG
IV access
sublingual GTN spray
aspirin 300mg
diamorphine IV + metaclopramide IV

?ticagrelor, clopidogrel or prasugrel

Glycoprotein IIb/IIIa inhibitors

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8
Q

What investigations would you do in ACS?

A

Bedside: ECG
Bloods: FBC U+E LFTs glucose lipids troponin I
Imaging: portable CXR

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9
Q

What are the indications for thrombolysis or PCI in STEMI?

A

<12hrs pain

\+ any of
ST elevation >1mm in 2 limb leads
ST elevation >2mm in 2 chest leads
posterior infarct
new onset LBBB
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10
Q

What are the absolute contraindications for thrombolysis?

A 
stroke <6m
CNS neoplasia
recent trauma or surgery
GI bleed <1m
bleeding disorder
aortic dissection
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11
Q

What are the relative contraindications for thrombolysis?

A

warfarin
pregnancy
advanced liver disease
infective endocarditis

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12
Q

State the complications of thrombolysis

A 
bleeding
hypotension
ICH
reperfusion arrhythmias
systemic embolisation of thrombus
allergic reaction
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13
Q

What drug is used for thrombolysis in STEMI?

A

reteplase

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14
Q

What are the complications of a STEMI?

A 
S udden death
P ericarditis
R upture papillary muscles
E mbolism
A rrhythmias
D ressler's syndrome
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15
Q

What drugs should a patient be prescribed post MI?

A 
Aspirin
ACEi
Beta blocker
Clopidogrel/prasugrel (STEMI)/ticegralor (NSTEMI)
Statin
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16
Q

In terms of work and driving, what should a patient be advised post MI?

A

off work for 1 month

need to inform DVLA - no driving for 1 month

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17
Q

How can you distinguish between NSTEMI and unstable angina?

A

troponin I 12hrs after onset
+ve for NSTEMI
-ve for unstable angina

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18
Q

How is an NSTEMI treated?

A

MONA

LMWH - fondaparinux
Beta blocker or calcium chanel blocker
nitrates

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19
Q

When should PCI be considered in a patient with NSTEMI?

A 
rise in troponin I
recurrent angina/ischaemic ECG changes despite therapy
heart failure develops
poor LV function
haemodynamically unstable
PCI <6m
previous CABG
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20
Q

Name some narrow complex tachycardias

A 
regular:
sinus tachy
accessory pathway
atrial tachy
junctional tachy - - AVNRT/AVRT
multifocal atrial tachycardia

irregular:
AF

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21
Q

How do you manage a regular narrow complex tachycardia?

A

ABC
O2
IV access

vagal manoeuvres
adenosine 6mg IV bolus
monitor ECG

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22
Q

How does adenosine work?

A

inhibition SAN and AVN

Leads to AV block

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23
Q

What are the vagal manouevres?

A

carotid sinus massage

Valsalva - hold breath and bear down

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24
Q

If adenosine fails, and the patient is haemodynamically compromised in regular SVT, what next?

A

Senior help!!!

Amiodarone 300mg IV
DC cardioversion

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25
Q

If adenosine fails, and the patient is haemodynamically stable in regular SVT, what next?

A

senior help!!!

B blocker
digoxin

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26
Q

What could cause a broad complex tachycardia?

A

VT - most common! until proven otherwise

SVT with BBB
SVT with aberrancy
WPW antidromic

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27
Q

If the patient is unstable, how should a VT be managed?

A

senior help!
sedation
DC cardioversion
amiodarone

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28
Q

If the patient is stable, how should a VT be managed?

A

amiodarone 300mg IV

If SVT, give adenosine

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29
Q

What is the most common organism to cause endocarditis?

A

Streptococcus viridans

Staph aureus in IVDU
Staphylococcus epidermidis in valve surgery <2m ago

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30
Q

What are the key features of infective endocarditis?

A

fever

new heart murmur

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31
Q

What murmurs are seen in infective endocarditis?

A

aortic regurg

mitral regurg

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32
Q

What are the systemic signs of infective endocarditis?

A

oslers nodes
janeway lesions
clubbing
splinter haemorrhages

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33
Q

What are the major criteria for diagnosis of IE?

A

+ve blood culture - typical organism on 2 separate cultures

evidence of endocardial involvement - +ve echo (vegetation, abscess, prosthetic valve damage) or new valvular regurgitation

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34
Q

What are the minor criteria for diagnosis of IE?

A 
predisposition - IVDU, prosthetic valve
fever >38
vascular signs
\+ve blood culture
\+ve echo
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35
Q

What predisposes to IE?

A 
prosthetic heart valves
congenital defect
valvular disease
prev endocarditis
prev rheumatic fever
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36
Q

What investigations if IE is suspected?

A

Bedside: ECG urinalysis
Bloods: FBC U+E LFT CRP
Micro: blood cultures X3
Imaging: CXR, Echo

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37
Q

Why is urinalysis done if IE is suspected?

A

glomerulonephritis can develop secondary to immune vasculitis

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38
Q

Treatment for IE

A

ABC
microbiologist + cardiologist
empirical abx - benzylpenicillin + gentamicin

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39
Q

How can you tell a posterior MI on an ECG?

A

reciprocal changes in V1-V3

ask for leads V7-V9

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40
Q

Which artery supplies the posterior aspect of the heart?

A

circumflex

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41
Q

What parts of the heart does the right coronary artery supply?

A

right atrium
right ventricle
SA Node
AV Node

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42
Q

What parts of the heart does the left anterior descending supply?

A

left ventricle
right ventricle
interventricular septum

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43
Q

What parts of the heart does the circumflex supply?

A

left atrium

left ventricle

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44
Q

What parts of the heart does the left marginal artery supply?

A

left ventricle

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45
Q

What parts of the heart does the right marginal artery supply?

A

right ventricle

apex

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46
Q

Which antiplatelet should be given to which groups of patients in the long term management of ACS

A

STEMI - aspirin + prasugrel
NSTEMI - aspirin + ticagrelor
other - aspirin + clopidogrel

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47
Q

List some complications of an MI

A 
Myocardium:
cardiac arrest - VF
cardiogenic shock
chronic heart failure
LV aneurysm

Electrics:
VT
AV block

Pericardium:
Pericarditis
Dressler’s syndrome

Valves:
mitral regurgitation

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48
Q

What is an LVAD?

What does it do?

A

Left Ventricular Assist Device
tube that pulls blood from the left ventricle into a pump. which sends blood into the aorta
Battery pack outside body

used in people with heart failure as long term therapy or bridge to transplant

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49
Q

What is a CRT-D?

What does it do?

A

Cardiac resynchronisation therapy - defibrillator

resynchronizes the contractions of the heart’s ventricles by sending tiny electrical impulses to the heart muscle, which can help the heart pump blood throughout the body more efficiently. Used in heart failure
Also cardioverter-defibrillator, to quickly terminate an abnormally fast, life-threatening heart rhythm

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50
Q

What is BNP used to measure?

A

BNP increases with right or left systolic or diastolic heart failure.
It is an independent predictor of high left ventricular end-diastolic pressure.
BNP levels decrease after effective treatment of heart failure.

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51
Q

When is BNP released?

A

in response to stretch of the ventricles

released in direct proportion to ventricular volume expansion and pressure overload

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52
Q

State the CHA2DS2-VASc score

A

C Congestive heart failure 1
H Hypertension (or treated hypertension) 1
A2 Age >= 75 years 2 Age 65-74 years 1
D Diabetes 1
S2 Prior Stroke or TIA 2
V Vascular disease (including ischaemic heart disease and peripheral arterial disease) 1
S Sex (female) 1

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53
Q

What counts as a vascular disease in CHA2DS2-VASc ?

A

ACS, PVD, MI, stent

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54
Q

What is the appropriate course of action in someone with a CHA2DS2-VASc score of 0?

A

no anticoagulation

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55
Q

What is the appropriate course of action in someone with a CHA2DS2-VASc score of 1?

A

Male - consider anticoagulation

Female - no anticoagulation

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56
Q

What is the appropriate course of action in someone with a CHA2DS2-VASc score of 2 or more?

A

Offer anticoagulation

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57
Q

What is the purpose of the HAS BLED score?

A

formalise this risk assessment of the risk of bleeding on anticoagulation medication

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58
Q

State the components of the HASBLED score

A

H Hypertension, uncontrolled, systolic BP > 160 mmHg 1

A Abnormal renal function (dialysis or creatinine > 200) 1 for any renal abnormalities
Or
Abnormal liver function (cirrhosis, bilirubin > 2 times normal, ALT/AST/ALP > 3 times normal 1 for any liver abnormalities

S Stroke, history of 1

B Bleeding, history of bleeding or tendency to bleed 1

L Labile INRs (unstable/high INRs, time in therapeutic range < 60%) 1

E Elderly (> 65 years) 1

D Drugs Predisposing to Bleeding (Antiplatelet agents, NSAIDs) 1 for drugs
Or
Alcohol Use (>8 drinks/week) 1 for alcohol

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59
Q

What can the HASBLED score tell you?

A

> =3 = high risk of bleeding

eg. intracranial haemorrhage, hospitalisation, haemoglobin decrease >2 g/L, and/or transfusion.

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60
Q

Where can AF conduct through?

A

AVN

accessory pathways

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61
Q

State some causes of AF

A 
HTN
ischaemia
cardiomyopathy
hyperthyroidism
mitral stenosis
obstructive sleep apnoea
CCF
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62
Q

State some drugs used for rate control in AF

A

bisoprolol

verapamil

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63
Q

State some drugs used for rhythm control in AF

A

flecainide
sotalol
amiodarone

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64
Q

When is flecainide contraindicated?

A

ischaemic heart disease
structural heart disease
valvular heart disease

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65
Q

In what groups of patients are NOACs not licensed for use?

A

prosthetic valves

mitral stenosis

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66
Q

When are NOACs indicated for prevention of stroke and systemic embolism in AF?

A

non-valvular disease

\+ one or more of:
prior stroke or transient ischaemic attack
age 75 years or older
hypertension
diabetes mellitus
heart failure
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67
Q

Name some NOACs

A

dabigatran
rivaroxiban
apixaban

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68
Q

What is the mechanism of action of the NOACs?

A

dabigatran + rivaroxaban = direct factor Xa inhibitors

apixaban = direct thrombin inhibitor

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69
Q

What length is a broad complex tachycardia?

A

> 120ms, >3 small squares

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70
Q

What is seen in VT on ECG?

A 
positive QRS concordance
LAD
AV dissociation or AV block
fusion beats
capture beats
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71
Q

What is a fusion beat?

A

= normal QRS + VT = unusual complex

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72
Q

What is a capture beat?

A

= normal QRS between abnormal beats

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73
Q

Which cardiac arrest rhythms are shockable?

A

VF

pulseless VT

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74
Q

Which cardiac arrest rhythms are non-shockable?

A

pulseless electrcal activty

asystole

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75
Q

What are the reversible causes of cardiac arrest?

A

hypoxia
hypovolaemia
hypo/hyperkalaemia
hypothermia

thrombosis
tamponade
toxins
tension pneumothorax

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76
Q

What is VT?

Why is it considered an emergency?

A

broad-complex tachycardia originating from a ventricular ectopic focus.

has potential to precipitate ventricular fibrillation

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77
Q

What causes monomorphic VT?

A

myocardial infarction

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78
Q

What causes polymorphic VT eg torsades de pointes?

A

prolongation of QT interval

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79
Q

Give some causes of QT interval prolongation

A 
sotalol
amiodarone
TCA
fluoxetine
hypocalcaemia
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80
Q

What is bifascicular block?

A

both the right bundle branch AND one of the left bundle branch fascicles is not conducting.

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81
Q

How is bifascicular block seen on ECG?

A

combination of RBBB with left anterior or posterior hemiblock
e.g. RBBB with left axis deviation

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82
Q

What is trifascicular block?

A

combination of RBBB with left anterior or posterior hemiblock
AND
1st degree heart block

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83
Q

What murmur is most likely to occur in and IVDU with IE?

A

Tricuspid regurg

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84
Q

What murmur is most likely to occur with IE?

A

mitral or aortic regurgitation

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85
Q

When is valve replacement considered in IE?

A

If the infection is not clearing despite optimal Abx

heart failure starts to develop

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86
Q

What is the difference between AVRT and AVNRT?

A

AVRT - accessory pathway between ventricles and atria

AVNRT - accessory pathway between AVN and atria
alpha = slow, beta = fast. causes loop

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87
Q

Give lifestyle interventions used in management of hypertension

A 
smoking cessation, 
weight reduction, 
reduction of excessive intake of alcohol and caffeine, 
reduction of dietary salt, 
reduction of total and saturated fat, 
increasing exercise,
increasing fruit and vegetable intake.
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88
Q

What investigations are carried out in suspected HTN?

A

clinicn BP >140/90

confirmed using ambulatory blood pressure monitoring or home blood pressure monitoring

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89
Q

What are some causes of secondary HTN?

A 
phaeochromocytoma
renal disease
pre-eclampsia
renal artery stenosis
Conn's
hyper/hypothyroid
coarctation aorta
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90
Q

Describe systolic heart failure

A

inability of the ventricles to contract to give sufficient cardiac output

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91
Q

Describe diastolic heart failure

A

inability of the ventricles to relax and fill to provide sufficient cardiac output

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92
Q

What can the ejection fraction tell us in heart failure?

A

<40% = systolic

> 50% = diastolic

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93
Q

What are the causes of systolic heart failure

A

IHD
dilated cardiomyopathy
MI

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94
Q

What are the causes of diastolic heart failure

A

constrictive periccarditits
tamponade
restrictive or hypertrophic cardiomyopathy
HTN

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95
Q

What are the causes of high output heart failure?

A

anaemia
pregnancy
hyperthyroidism

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96
Q

What are the symptoms of left heart failure?

A 
breathlessness, 
reduced exercise tolerance, 
PND, 
orthopnoea, 
fatigue, 
nocturnal cough, 
wheeze, 
nocturia, 
weight loss.
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97
Q

What are the signs of left heart failure?

A 
cool peripheries, 
muscle wastage, 
crepitations on auscultation, 
S3 gallop, 
pleural effusion, 
displaced apex beat due to LV dilatation, 
Low BP,
narrow pulse pressure due to low stroke volume,
tachycardia,
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98
Q

What are the symptoms of right heart failure?

A

peripheral pitting oedema
ascites
nausea
anorexia

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99
Q

What are the signs of right heart failure?

A 
Neck vein distension, 
S3 gallop, 
raised JVP, 
hepatomegaly, 
hepatojugular reflex,
RV heave
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100
Q

How should a person with suspected heart failure be investigated if they have had a previous MI?

A

Bedside: ECG
Bloods: U+E, eGFR, FBC, TFT, LFT, HbA1c, and fasting lipids.
Imaging: echo within 2 weeks, CXR
Refer: specialist

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101
Q

How should a person with suspected heart failure be investigated if they have not had a previous MI?

A

Bedside: ECG
Bloods: BNP!!! U+E, eGFR, FBC, TFT, LFT, HbA1c, and fasting lipids.
Imaging: CXR, echo

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102
Q

How does the management of heart failure change depending on BNP level?

A

If the BNP level is above 400 pg/mL refer for specialist assessment and echocardiography to be seen within 2 weeks.
If the BNP level is between 100-400 pg/mL, refer for specialist assessment and echocardiography to be seen within 6 weeks.
If BNP levels are less than 100 pg/mL a diagnosis of heart failure is unlikely. Consider referral if a clinical suspicion of heart failure persists and conditions are present which may cause a false negative result.

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103
Q

What can cause a false negative BNP result?

A 
Obesity
Diuretics
ACE inhibitors
Beta-blockers
Angiotensin 2 receptor blockers
Aldosterone antagonists
104
Q

What can cause a increase the levels of BNP?

A

Age over 70 years.
Female gender.
Left ventricular hypertrophy, myocardial ischaemia, or tachycardia.
Hypoxia.
Pulmonary hypertension.
Pulmonary embolism.
Chronic kidney disease (estimated glomerular filtration rate less than 60 mL/min/1.73m2).
Sepsis.
Chronic obstructive pulmonary disease (COPD).
Diabetes mellitus.
Liver cirrhosis.

105
Q

What is BNP?

A

BNP is a biologically active peptide and has vasodilator and natriuretic properties released from the cardiac ventricles in response to stretching of the chamber.

The release of BNP appears to be in direct proportion to ventricular volume expansion and pressure overload. BNP increases with right or left systolic or diastolic heart failure. It is an independent predictor of high left ventricular end-diastolic pressure. BNP levels decrease after effective treatment of heart failure.

106
Q

Describe the New York Heart Association classification of class I heart failure

A

no symptoms

no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations

107
Q

Describe the New York Heart Association classification of class II heart failure

A

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

108
Q

Describe the New York Heart Association classification of class III heart failure

A

moderate symptoms

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

109
Q

Describe the New York Heart Association classification of class IV heart failure

A

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

110
Q

What is the management of heart failure?

A

first-line = ACE-inhibitor + beta-blocker
second-line = aldosterone antagonist, angiotensin II receptor blocker or a hydralazine in combination with a nitrate
third line = cardiac resynchronisation therapy or digoxin

diuretics should be given for fluid overload

offer annual influenza vaccine
offer one-off** pneumococcal vaccine

cardiac rehabilitation

111
Q

Which beta blockers are suitable to use in heart failure?

A

bisoprolol, carvedilol, and nebivolol.

112
Q

Which drugs can worsen pre-existing heart failure?

A

NSAIDs,
beta-blockers,
calcium-channel blockers`.

113
Q

What are the symptoms of pericarditis

A

chest pain - improves on sitting forwards, worse on inspiration
SOB
non-productive cough
flu like

114
Q

What are the signs of pericarditis

A

pericardial friction rub
tachycardia
tachypnoea
fever

115
Q

What can cause pericarditis

A 
idiopathic
coxsackie b
Dressler's syndome
uraemia
systemic - RA, SLE
TB
116
Q

How should suspected pericarditis be investigated?

A

bedside: ECG
bloods: FBC, U+E, troponin I , autoantibodies
Mirco - blood cultures, viral serology
Imaging: CXR, echo

117
Q

What are the signs on ECG of pericarditis

A

widespread ST elevation
PR depression
T wave inversion/depresssion

118
Q

What is a complication of pericarditis

A

pericardial effusion

119
Q

How is pericarditis treated

A

analgesia

treat cause

120
Q

What is the sign of pericardial effusion on CXR

A

water bottle heart

121
Q

what is the sign of pericardial effusion on ECG

A

electical alternans

122
Q

What is constrictive pericarditis

A

heart encased in rigid pericardium

123
Q

Pericarditis can lead to constrictive pericarditis. What is a major cause of constrictive pericarditis

A

TB

124
Q

What are the symptoms of constrictive pericarditis

A

dyspnoea

oedema

125
Q

What are the signs of constrictive pericarditis

A

right heart failure: elevated JVP, ascites, oedema, hepatomegaly
Kussmaul’s sign
pericardial knock
third heart sound

126
Q

What is Kassmaul’s sign

A

JVP rising paradoxically with inspiration`

127
Q

What is seen on CXR in constrictive pericarditis

A

pericardial calcification

128
Q

How is the JVP changed in cardiac tamponade

A

absent Y descent

tamponade = TAMpaX

129
Q

What are the signs of cardiac tamponade

A 
dyspnoea
tachycardia
hypotension
muffled heart sounds
raised JVP
pulsus paradoxus
130
Q

What is pulsus paradoxus

A

abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration

131
Q

What is Beck’s triad?

A

cardiac tamponade:
falling BP
rising JVP
muffled heart sounds

132
Q

What investigations should be done in cardiac tamponade

A

Bedside: ECG
Imaging: CXR, echo

133
Q

What is the management of cardiac tamponade

A

urgent drainage!

134
Q

Define AF

A

irregular atrial electrical activity causing disorganised atrial depolarisations and ineffective contractions
due to the AVN receiving more impulses than it can conduct, the ventricular rate is irregular

135
Q

Define paroxysmal AF

A

lasting less than 7d, self terminating

136
Q

Define persistent AF

A

lasting >7days, terminates with cardioversion

137
Q

Define permanent AF

A

fails to terminate

138
Q

What investigations should be carried out in suspected AF?

A

ECG
FBC, U+E, troponin, TFT,
echo

139
Q

What are the main aims of treatment in AF

A

rate/rhythm control

stroke prevention

140
Q

Describe situations where rate or rhythm control are more suitable in the treatment of AF

A

rate - first line.

rhythm - if easily reversible cause, HF, new onset AF

141
Q

When can digoxin be used in the treatment of AF

A

as rate control in patients with HF or who are mianly sedentary

due to it being less effective at controlling the heart rate during exercise

142
Q

State Virchow’s triad

A

hypercoaguability
stasis
vessel wall injury

143
Q

State what Well’s score is used for

A

to determine the likelihood of a DVT

144
Q

State the factors involved in calculating a well’s score

A 
Active cancer (treatment ongoing, within 6 months, or palliative)	1
Previously documented DVT	1

Paralysis, paresis or recent plaster immobilisation of the lower extremities 1
Recently bedridden for 3 days or more or major surgery within 12 weeks requiring general or regional anaesthesia 1

Entire leg swollen 1
Calf swelling at least 3 cm larger than asymptomatic side 1
Pitting oedema confined to the symptomatic leg 1

Localised tenderness along the distribution of the deep venous system 1
Collateral superficial veins (non-varicose) 1

An alternative diagnosis is at least as likely as DVT -2

145
Q

How does management of DVT chnage depending on the outcome of the Well;s score

A

<2 = perform a D-dimer test
ifit is positive arrange:
a proximal leg vein ultrasound scan within 4 hours
(if a proximal leg vein ultrasound scan cannot be carried out within 4 hours low-molecular weight heparin should be administered whilst waiting)

> =2 = a proximal leg vein ultrasound scan should be carried out within 4 hours
if the result is negative, a D-dimer test
(if a proximal leg vein ultrasound scan cannot be carried out within 4 hours a D-dimer test should be performed and low-molecular weight heparin administered whilst waiting)

146
Q

How is a DVT treated?

A

enoxaparin 1.5mg/kg/24h or fondaparinux

warfarin for 3 months if provoked, 6m if unprovoked, lifelong if recurrent

stop LMWH when INR is 2-3 for 24hrs

147
Q

How should patients with an unprovoked DVT be investigated

A

a physical examination (guided by the patient’s full history) and
a chest X-ray and
blood tests (full blood count, serum calcium and liver function tests) and urinalysis.
CT CAP if >40y
thrombophilia screening if family history

148
Q

What are the signs of heart failure on CXR

A 
Alveolar oedema
Kerley B lines
Cardiomegaly
Dilated prominent upper lobe vessels
pleural Effusion
149
Q

What are the symptoms of aortic stenosis?

A

syncope
angina
dyspnoea

dizziness

150
Q

What are the causes of aortic stenosis

A

degenerative calcification
bicuspid valve
rheumatic fever

151
Q

What are the signs of aortic stenosis

A 
slow rising pulse
wide pulse pressure
heaving apex beat
ejection click
soft S2
ejection systolic murmur radiating to carotids
152
Q

How is aortic stenosis investigated?

A

ECG
FBC, U+E, cholesterol, glucose
CXR, echo, doppler echo

153
Q

What are the signs of aortic stenosis on ECG

A

p mitrale
LAD
LBBB

154
Q

What are the signs of aortic stenosis on CXR

A

LVH

calcified aortic valve

155
Q

Who is aortic valve replacement offered to in aortic stenosis

A

those who are symptomatic

asymptomatic, but valvular pressure gradient >40mmHg + LV dysfunction

156
Q

Who is ballon valvuloplasty offered to in aortic stenosis

A

those who need a replacement but are unfit for valve replacement

157
Q

What is an important differential for aortic stenosis

A

hypertrophic cardiomyopathy

158
Q

What is the appropriate management for asymptomatic aortic stenosis

A

monitoring every 6 months

stress test and echo

159
Q

in patients unfit for any surgical treatment, how should aortic stenosis be treated

A

tx of HTN or HF

160
Q

What are the causes of aortic regurgitation

A

valve insufficiency - IE, rheumatic fever, SLE

aortic root dilation - aortic dissection, HTN, ankylosing spondylitis, marfan’s, ehlers-danlos

161
Q

What are the symptoms of AR

A

dyspnoea
PND
orthopnoea

162
Q

What are the signs of aortic regurgitations

A 
collapsing pulse
wide pulse pressure
hyperdynamic apex beat
early diastolic murmur
S3
Quinke's
de Musset's
corrigan's
pistol shot femorals
163
Q

What is Quinke’s sign

A

visible pulsation in nail beds due to AR

164
Q

What is de Musset’s sign

A

head bobbing in time with pulse in AR

165
Q

What is corrigan’s sign

A

visible carotid pulsations in AR

166
Q

What investigations should be carried out in AR

A

ECG
FBC
blood cultures
CXR, echo

167
Q

What is seen on CXR in AR

A

cardiomegaly
aortic dissection
pulmonary oedema

168
Q

What is seen on ECG in AR

A

LAD

increased R wave amplitude in aVL, I, V4-6

169
Q

Where is the AR mumur heard best

A

leaning forwards in expiration at lower left sternal edge

170
Q

What is the treatment for AR

A

conservative - ACEi - to decrease symptoms.review every 6m with echo

surgical - replacement or balloon valvuloplasty

171
Q

What are the indications for surgery in aortic regurgitation

A

incrreasing symotoms
enlarging heart
ECG deterioration
IE refractory to medical therapy

172
Q

what are the causes of mitral stenosis

A

rheumatic fever

173
Q

what causes rheumatic fever

A

2-6 weeks post Streptococcus pyogenes infection

molecular mimicary means there is immune targeting of the heart tissue

174
Q

what are the symptoms of mitral stenosis

A

exertional dyspnoea
PND
orthopnoea
palpitations

175
Q

Why does mitral stenosis cause RHF

A

increased pressure in the left atrium leads to venous congestions and pulmonary hypertension
right heart failure

176
Q

Why does mitral stenosis cause AF

A

stretch of myocytes
irritation
AF!

177
Q

What are the signs of mitral stenosis

A 
low volume pulse
AF
mitral facies
tapping non-displaced apex beat
opening snap
mid-late diastolic murmur

Right ventricular heave
raised JVP
bibasal crackles
peripheral oedema

178
Q

Where is the murmur in mitral stenosis best heard

A

in mitral area lying on left during expiration with bell

179
Q

What investigations should be carried out in mitral stenosis

A

ECG
CXR
echo

180
Q

What is seen on CXR in mitral stenosis

A

left atrial enlargement
double right heart border
elevation of left bronchus

181
Q

What is the treatment for mitral stenosis

A

conservative: diuretics, rate control and anticoagulation in AF, yearly follow up with echo
surgical: Percutaneous mitral commissurotomy (PMC) or mechanical valve replacement

182
Q

When is surgery indicated for mitral stenosis

A

severe

pulmonary hypertension

183
Q

What are the causes of mitral regurgitation

A

primary = damage to valve
IE, rheumatic fever, papillary muscles damaged in MI

secondary = due to left ventricular dilation, valve incompetency results.
idiopathic cardiomyopathy or coronary heart disease, left heart failure

184
Q

What are the symptoms of mitral regurgitation

A

dyspnoea

fatigue

185
Q

What are the signs of mitral regurgitation

A 
AF
displaced hyperdynamic apex beat
soft S1
split S2
pansystolic murmur
186
Q

What investigations should be carried out in mitral regurgitation

A

ECG
CXR
echo

187
Q

What are the signs of mitral regurgitation on CXR

A

left atrial and ventricular enlargement

pulmonary oedema

188
Q

What is the treatment for mitral regurgitation?

A

conservative: rate control and anticoagulation for AF, diuretics and ACEi for pulmonary oedema
surgical: valve replacement or repair

189
Q

When is surgery indicated in mitral regurgitation

A

signs of left ventricular dysfunction, symptoms bad

190
Q

where is mitral regurgitation murmur radiate to?

A

the axilla

191
Q

What are some risk factors for ischaemic heart disease

A

Increasing age
Male gender
Family history

Smoking
Diabetes mellitus
Hypertension
Hypercholesterolaemia
Obesity
192
Q

State the pathophysiology of IHD

A

initial endothelial dysfunction
fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
monocytes migrate from the blood and differentiate into macrophages.
macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’.
smooth muscle proliferation and migration from the tunica media into the intima
formation of a fibrous capsule covering the fatty plaque.

193
Q

Describe the pathophysiology of angina

A

the plaque forms a physical blockage in the lumen of the coronary artery.
This may cause reduced blood flow and hence oxygen flow to the myocardium, particularly at times of increased demand

194
Q

What are the potential systemic consequences of infective endocarditis

A

Cerebrovascular accident (CVA) from embolism
Finger/toe gangrene caused by embolism ± vasculitis.
• Renal or splenic abscess or infarction.
• Mesenteric embolism (ischaemic bowel and an acute abdomen).
• Joint infection.
• Bone infection
• Acute renal failure: this may occur from immune complex disease, haemodynamic upset (acute heart failure), damage during cardiac surgery and nephrotoxic antibiotics. Close monitoring of renal function throughout the illness is mandatory

195
Q

When would surgery be indicated in infective endocarditis

A

Severe valvular destruction causing heart failure.
• Abscess formation.
• Failure to eradicate infection despite prolonged antibiotic therapy.
• Prosthetic valve endocarditis.

196
Q

Describe the pathophysiology of infective endocarditis

A

damaged valve endothelium
thrombosis (fibrin and platelets aggregate)
bacterial adhesion to form biofilm = vegetation

197
Q

Where could the bacterial source be in IE

A

open wound
mouth - poor dentition
gut - more likely if colorectal cancer or UC
IVDU

198
Q

Describe the characteristic signs of WPW on ECG

A

short PR interval
slurring QRS
delta wave

199
Q

Why is there shortening of the PR interval and a delta wave in WPW

A

atrioventricular reentrant pathway means that excitation passes from the atria to the ventricles more quickly than through the AVN

this means the PR interval is shortened

the excitation travels slowly through the myocardium, which is why the slurred upstroke (delta wave) occurs

200
Q

What is used to treat an SVT in the long term?

A

B blocker or digoxin as prophylaxis

radiofrequency ablation to cure

201
Q

What are the differences between a monomorphic VT and a polymorphic VT

A

mono
caused by structural problem
does not often convert to VF
uniform QRS complexes

poly
caused by metabolic or electrophysiological lengthening of QT interval
quickly converts to VF
less regular and chaotic QRS complexes

202
Q

What is the treatment for polymorphic VT

A

stop drugs that prolong QT interval
correct metabolic abnormalities
IV magnesium sulfate 2mg over 10mins

203
Q

What class as adverse features in tavhycardia

A

shock
syncope
myocardial ischaemia
heart failure

204
Q

What are the possoble signs of ACS on CXR

A

pulmonary oedema

cardiomegaly

205
Q

What are the signs of heart failure on CXR

A 
alveolar oedema
Kerley B lines
Cardiomegaly
upper lobe diversion
pleural effusion
206
Q

What is the role of palliative care in severe heart failure?

A

40% die within in a year of diagnosis
need to educate, advande care plan
prescibe meds for pain and symptoms relief - opiates and O2 help

207
Q

How can you distinguish between tricuspid and mitral regurgitation

A

mitral - pansystolic radiating to axilla

tricuspid - pansystolic heard best in inspiration at the lower sternal edge

208
Q

What is mitral valve prolapse?

A

mitral valave leaftlets bulge into left strium during ventricular systole

209
Q

What can cause mitral valve prolapse

A

ASD
patent ductus srteriosis
cardiomyopathy
Marfan’s

210
Q

What are the signs of mitral valve prolapse

A

mid systolic click

late systolic murmur

211
Q

To which patients with mitral valve prolapse should prophylactic antibiotics be given to?

A

A systolic click and murmur on examination.

Myxomatous degeneration and mitral regurgitation on echocardiography.

‘High-risk’ features, such as LV dilatation, left atrial enlargement, leaflet thickening, redundant chordae,
Age over 50, hypertension or obesity.
Moderate-to-severe mitral regurgitation.
Mitral regurgitation during exercise but not at rest.
Echocardiographic findings of mitral leaflet thickness >5 mm, posterior leaflet prolapse or increased LV dimensions.
Atrial fibrillation.
Reduced LV systolic function.
Left atrial enlargement.

212
Q

What are the key questions to ask a patient with HTN

A 
changes in vision
kidney problems - haematuria?
sweating/palpitations? - phaeochromocytoma
weight gain? - Cushing's
diabetic?
CV disease
smoking, alcohol
medications
213
Q

What signs are present in HTN

A

LVH
retinopathy
palpable kidneys - renal disease
signs of Cushing’s or hyperthyroid

214
Q

What are the causes of HTN

A

primary essential

secondary:
Cushing's
renal
Conn's
phaeochromocytoma
coarctation of the aorta
drugs: steroids, COCP, NSAIDs
215
Q

What is a normal BP

A

<140/90

216
Q

Define the korotkov sounds

A

sounds heard when auscultating manual blood pressure reading between systolic and diastolic pressure

217
Q

What are the 5 kortokov sounds

A 
1 = tapping
2 = soft swishing
3 = crisp
4 = blowing
5 = silence
218
Q

What are eh features of ohypertensive retinopathy

A

arteriolar narroqing
etinal haemorrhages
papilloedema
cotton wool spots

219
Q

What are the key investigations in HTN

A

24 hour ambulatory BP, urine dipstick, ECG
FBC, U+E, glucose, lipid profile,
urine catecholamines, urine free cortisol
USS kidneys

220
Q

What is the difference between arteriosclerosis and atherosclerosis

A

Arteriosclerosis is the stiffening or hardening of the artery walls.

Atherosclerosis is the narrowing of the artery because of plaque build-up. It is a type of arteriosclerosis

221
Q

When should antihypertensive medication be considered?

A

if Stage 2

or

 if < 80 years of age AND
target organ damage, 
established cardiovascular disease, 
renal disease, 
diabetes 
10-year cardiovascular risk equivalent to 20% or greater
222
Q

Define Stage 1 HTN

A

Clinic BP >= 140/90 mmHg

ABPM daytime average or HBPM average BP >= 135/85 mmHg

223
Q

Define stage 2 HTN

A

Clinic BP >= 160/100 mmHg

ABPM daytime average or HBPM average BP >= 150/95 mmHg

224
Q

If the clinic reading of BP is >140/90, what is the next step

A

ABPM or HBPM

225
Q

What are the complications of untreated HTN

A 
stroke
AF
MI
PVD
CKD
HF
retinopathy
AAA
vascular dementia
226
Q

What are the stages in management of HTN

A

Step 1 treatment
< 55-years-old: ACE inhibitor
>= 55-years-old or of Afro-Caribbean origin: calcium channel blocker

Step 2 treatment
ACE inhibitor + calcium channel blocker (A + C)

Step 3 treatment
add a thiazide diuretic (D)
chlorthalidone or indapamide

Step 4 treatment
consider further diuretic treatment
if potassium < 4.5 mmol/l add spironolactone 25mg od
if potassium > 4.5 mmol/l add higher-dose thiazide-like diuretic treatment

227
Q

What is resistant HTN

A

clinic BP >= 140/90 mmHg after step 3 treatment with optimal or best tolerated doses

228
Q

What is teh blood pressure target in HTN

A

<140/90 if <80y

<150/90 if >80y

229
Q

What are ACEi used for?

A

HTN
kidney protection in diabetes
post MI
HF

230
Q

What is the mechanism of action of ACEi

A

Inhibit the conversion angiotensin I to angiotensin II therefore causing vasodilation
and preventing aldosterone release

reduces BP

231
Q

What are teh common adverse effects of ACEi

A

dry cough
angioedema
hyperkalaemia

232
Q

Why might ACEi be contraindicated

A

hypersensitivity to ACEi

233
Q

What is bisoprolol used for

A

HF

angina

234
Q

What are some contraindications for beta blockers

A 
Asthma; - risk of bronchspasm
cardiogenic shock; 
hypotension; 
marked bradycardia; 
second or third-degree AV block; 
severe peripheral arterial disease;
uncontrolled heart failure
235
Q

What are some things to be careful of in treatment with loop diuretics?

A

Elderly - particularly susceptible to the side-effects.

Potassium loss - In hepatic failure, hypokalaemia caused by diuretics can precipitate encephalopathy, particularly in alcoholic cirrhosis.

Urinary retention - If there is an enlarged prostate, urinary retention can occur

236
Q

What info should be given to patients about loop diuretics

A

may cause dizziness, electrolyte abnormalities, tummy upset

need to have blood tests to monitor electrolyte levels

best taken in morning - so that not weeing during night! you may find you need to go to the toilet a couple of times within a few hours of taking the tablet.

237
Q

What kind of drug is simvastatin

A

inhibitor of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis
lowers cholesterol

238
Q

When should statins be taken? Why?

A

before bed

most cholesterol is made at night

239
Q

What are the side effects of statins

A

myalgia
rarely - myositis, rhabdomyolysis
liver impairment

240
Q

What monitoring should take place in statin therapy

A

checking LFTs at baseline, 3 months and 12 months.

baseline CK and lipid profile

241
Q

What can cause bradycardia

A

physiological (e.g. during sleep, in athletes)
cardiac causes (e.g. atrioventricular block or sinus node disease)
non-cardiac causes (e.g. vasovagal, hypothermia, hypothyroidism, hyperkalaemia)
drugs (e.g. beta-blockade, diltiazem, digoxin, amiodarone) in therapeutic use or overdose.

242
Q

What defines bradycardia

A

HR <60BPM

243
Q

Describe the management of bradycardias

A

A-E assessment

if signs of adverse features, give atropine 500mcg IV
if unsuccessful, arrange senior help and transvenous pacing

if no adverse features, assess for risk of asystole

if risk of asystole, ger senior help and arrange transvenous pacing

244
Q

What are the adverse features of bradycardias

A

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

245
Q

What is the mechanism of action of atropine

A

o antagonises acetylcholine at postganglionic nerve endings

o increases sinus rate and sinoatrial and AV conduction.

246
Q

What makes a patient at risk of asystole in bradycardia

A

previous asystole
Mobitz II heart block
complete heart block
ventricular pause >3s

247
Q

What are some interim measures that you can do whilst waiting for transvenous pacing in bradycardia

A

further atropine up to 3mg
transcutaenous pacing
adrenaline

248
Q

What is a PDA

A

patent ductus arteriosus

between descending aorta and pulmonary trunk

249
Q

What are the signs of PDA

A

continuous machinery murmur
left supraclavicular palpable thrill
wide pulse pressure
collpasing pulse

250
Q

What are the signs of ASD

A

ejection systolic murmur

251
Q

What are the signs of coarctation of the aorta

A

radiofemoral delay
HTN
midsystolic murmur

252
Q

What are the INR targets for pts taking warfarin

A

venous thromboembolism: target INR = 2.5, if recurrent 3.5

atrial fibrillation, target INR = 2.5

mechanical heart valves, target INR depends on the valve type and location. Mitral valves generally require a higher INR than aortic valves.

253
Q

Describe the pathophysiology of aortic dissection

A

tear in tunica intima

high pressure in artery forces blood between tunica intima and tunica media to form a fulse lumen

254
Q

What is the difference between Type A and B aortic dissections

A 
A = ascending
B =  descending dital to subclavian
255
Q

What are some causes of aortic dissection

A

HTN
CT disease - Ehler’s-danlos or Marfan’s
aneurysms

256
Q

What are the symptoms and signs of aortic dissection

A

chest pain - tearing, radiating to back
weak pulses
hypotension
AR

257
Q

What is the long term management of acute heart failure

A

Daily weights, aim reduction of 0.5kg/day
Repeat CXR.
• Change to oral furosemide or bumetanide.
• If on large doses of loop diuretic, consider the addition of a thiazide (eg bendroflumethiazide or metolazone 2.5–5mg daily po).
• ace-i if lvef <40%. If ace-i contraindicated, consider hydralazine and nitrate (may also be more effective in African-Caribbeans).
• Also consider β‎-blocker and spironolactone (if lvef <35%).
• Is the patient suitable for biventricular pacing or cardiac transplantation?
• Optimize management of AF if present; consider anticoagulation.

Finals (32 decks)

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