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cardiovascular Flashcards

1
Q

CXR in aortic dissection

A

Widened mediastinum
Double aortic contour
Irregular aortic contour
Inward displacement of atherosclerotic calcification

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2
Q

CT angiography aortic dissection

A

False lumen

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3
Q

ix for aortic dissection

A

CXR

CT angiography is the initial ix - diagnostic

Transoesophageal echocardiography (TOE) - espesh if unstable

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4
Q

types of aortic dissection

A

type A - ascending aorta, 2/3 of cases - worse prog

type B - descending aorta, distal to left subclavian origin, 1/3 of cases

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5
Q

mx aortic dissection for type A + B

A

Type A
surgical management - control BP to a target systolic of 100-120 mmHg whilst waiting

Type B
conservative management
- bed rest
reduce blood pressure IV labetalol

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6
Q

murmur for aortic stenosis

A

ejection systolic
(louder on expiration)

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7
Q

murmur for mitral regurgitation

A

pan-systolic

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8
Q

presentation of aortic dissection

A

50+ men

sudden onset tearing chest pain radiating to the back

radio-radial delay
radio-femoral delay
BP diff between arms

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9
Q

RF aortic dissection

A

Hypertension
Connective tissue disease e.g. Marfan’s syndrome
Valvular heart disease
Cocaine/amphetamine use

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10
Q

who is at risk of having a silent MI

A

px w DM

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11
Q

ECG changes for hypercalcaemia

A

shorted QT interval
J waves if severe

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12
Q

what is Wellen’s syndrome and what are the signs of it

A

characterised by biphasic or deeply inverted T waves in V2-3

history of recent chest pain now resolved (cardiac ischaemia in the setting of unstable angina)

highly specific for critical stenosis of the left anterior descending artery (LAD)

  • high risk needing further ix
    Troponin normal at this stage
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13
Q

immediate ACS drug therapy

A
  • aspirin 300mg
  • oxygen should only be given if the patient has oxygen saturations < 94%
  • morphine should only be given for patients with severe pain
  • nitrates,useful if the patient has ongoing chest pain or hypertension, should be used in caution if patient hypotensive
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14
Q

mx of STEMI

A

PCI - if the presentation is within 12 hours of the onset of symptoms AND can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI)

fibrinolysis (w/ eg alteplase) - should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given

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15
Q

further drug therapy before PCI

or if not taking an anticoag
if taking an anticoag

A

‘dual antiplatelet therapy’, i.e. aspirin + another drug

if the patient is not taking an oral anticoagulant: prasugrel
if taking an oral anticoagulant: clopidogrel

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16
Q

fibrinolysis/thrombolysis what to do before and after

A

give another antithrombin drug

An ECG should be repeated after 60-90 minutes to see if the ECG changes have resolved. If patients have persistent myocardial ischaemia following fibrinolysis then PCI should be considered.

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17
Q

when to give heparin in NSTEMI/unstable angina

A

if immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given

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18
Q

which px w NSTEMI get angiography? (w follow on PCI if needed)

A

immediate: patient who are clinically unstable (e.g. hypotensive)

within 72 hours: patients with a GRACE score > 3% i.e. those at intermediate, high or highest risk

coronary angiography should also be considered for patients if ischaemia is subsequently experienced after admission

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19
Q

Risk assessment tool for ACS

A

GRACE

age
heart rate, blood pressure
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels

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20
Q

how to terminate supraventricular tachycardias

A

vasovagal maneuvers if haemodynamically stable

12mg adenosine via large bore cannula (as they are narrow complex)

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21
Q

what are the ECG changes in a posterior MI?

A

reciprocal changes to STEMI
changes in V1-3
- horizontal ST depression
- tall, broad R waves
- upright T waves
- dominant R wave in V2

see tall R waves? Right behind you!

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22
Q

what artery is affected in posterior MI?

A

left circumflex

(sometimes right coronary)

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23
Q

where is the lesion if someone gets complete heart block after an MI

A

right coronary artery (as it supplies the AV node)

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24
Q

triad for cardiac tamponade (pericardial tamponade)

A

Beck’s triad
- hypotension
- muffled/distant heart sounds
- elevated JVP

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25
Q

tx of cardiac tamponade

A

urgent pericardiocentesis (pericardial needle aspiration)

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26
Q

classic presentation of myocarditis

A

Patients are usually <50
hx of recent viral illness

chest pain and features of pulmonary oedema

inflammatory markers and troponin will be raised, and ECG will show non-specific ST segment and T wave changes

Myocarditis can manifest as new-onset congestive heart failure

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27
Q

6 ps of acute limb ischaemia

A

Pulseless
Painful
Pale
Paralysis
Paraesthesia
Perishingly cold

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28
Q

what blood test indicates right ventricular failure

A

Raised NT‑proBNP

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29
Q

causes of pericarditis

A

idiopathic
infection - TB, HIV, coxsacki, EBV etc
AI + inflam conditions - SLE, RA
injury - after MI, surgery, trauma
uraemia 2ndary to renal impairment
cancer
meds - methotrexate

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30
Q

what is pericarditis

A

inflam of the pericardium (membrane surrounding heart)

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31
Q

what is pericardial effusion

A

when the potential space of the pericardial cavity fills w fluid - creates an inward pressure on the heart making it harder to expand during diastole

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32
Q

pericarditis presentation

A

chest pain - sharp, central/anterior, pleuritic, worse when lying down, better when sitting forward
low grade fever

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33
Q

on auscultation w pericarditis

A

pericardial friction rub - rubbing scratching sound occurring alongside heart sounds

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34
Q

ix for pericarditis

A

Raised inflam markers -WBCs, CRP, ESR

ECG
- saddle shaped ST-elevation
- PR depression (more specific)

Echo to dx pericardial effusion

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35
Q

mx pericarditis

A

NSAIDs - aspirin / ibuprofen

colchicine (longer term to reduce recurrence)

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36
Q

what is cardiac tamponade (pericardial tamponade)

A

when the pericardial effusion is large enough to raise the intra-pericardial pressure squeezing the heart. Decreases CO. Emergency needing prompt drainage (pericardiocentesis)

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37
Q

what is infective endocarditis

A

infection of the endocardium (inner surface of the heart). Most commonly affecting heart valves

acute, subacute or chronic

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38
Q

RFs for endocarditis

A

IV drug use
CKD
Immunocompromised
Hx of it
Structural heart pathology
- valvular HD
- congenital HD
- hypertrophic cardiomyopathy
- prosthetic valves
- implantable devices

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39
Q

most common cause of endocarditis

A

most common is staph aureus

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40
Q

presentation of endocarditis

A

F fever
R roth spots (haemorrhages on retina in fundoscopy)
O osler nodes (tender red/purple nodules on pads of fingers + toes)
M murmur (new or changing)

J janeway lesions (painless red flat macules on palms or soles)
A anaemia
N nail-bed haemorrhages
E emboli

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41
Q

endocarditis ix

A

blood cultures - needed b4 abx
3 blood samples separated by 6 hrs + taken at diff sites

ECHO (TOE) - vegetations on valves

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42
Q

Dukes criteria for dx endocarditis

A

A diagnosis requires either:
- One major plus three minor criteria
- Five minor criteria

Major criteria are:
- Persistently positive blood cultures (typical bacteria on multiple cultures)
- Specific imaging findings (e.g., a vegetation seen on the echocardiogram)

Minor criteria are:
- Predisposition (e.g., IV drug use or heart valve pathology)
- Fever above 38°C
- Vascular phenomena (e.g., splenic infarction, intracranial haemorrhage and Janeway lesions)
- Immunological phenomena (e.g., Osler’s nodes, Roth spots and glomerulonephritis)
- Microbiological phenomena (e.g., positive cultures not qualifying as a major criterion)

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43
Q

endocarditis abx + how long

A

Initial IV broad spectrum abx - amoxicillin (vancomycin if penicillin allergic) + optional gentamicin
Ctu
- 4 weeks (6 wks if prosthetic heart valves)

If prosthetic valve
vancomycin + rifampicin + low-dose gentamicin

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44
Q

common cause of sudden cardiac death in young ppl

A

hypertrophic obstructive cardiomyopathy (HOCM) / left ventricular outflow tract obstruction

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45
Q

HOCM inheritance

A

AD

defect in the genes for sarcomere proteins

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46
Q

HOCM presentation

A

mostly asx

Non-specific sx
- SOB, fatigue, dizzy, syncope, chest pain, palp

Severe: sx of HF

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47
Q

ix for HOCM

A

ECG - left ventricular hypertrophy (large R waves in L sided leads, v5 v6 avL I, deep S waves in R sided chest leads, v1 v2)
- maybe T wave inversion

CXR - normal / pulmonary oedema

echo for dx

genetic testing

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48
Q

mx HOCM

A
  • Beta blockers
  • Surgical myectomy (removing part of the heart muscle to relieve the obstruction)
  • Alcohol septal ablation (a catheter-based, minimally invasive procedure to shrink the obstructive tissue)
  • Implantable cardioverter defibrillator (for those at risk of sudden cardiac death or ventricular arrhythmias)
  • Heart transplant
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48
Q

what sld be avoided in HOCM

activities
and meds

A

Patients are advised to avoid intense exercise, heavy lifting and dehydration.

ACE inhibitors and nitrates are avoided as they can worsen the LVOT obstruction.

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49
Q

which meds can reduce BNP levels

A

tx w ACEis
ARBs
diuretics

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50
Q

what can raise BNP

A

heart failure (high sensitivity varied specificity)

+ any cause of left ventricular dysfunction such as myocardial ischaemia or valvular disease

due to reduced excretion in px w CKD

PE
sepsis
COPD
tachycardia

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51
Q

ix results in left ventricular aneurysm

A

persistent ST elevation after MI

3rd + 4th heart sound

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52
Q

common finding in takayusu’s arteritis (a large vessel vasculitis)

A

absent limb pulse

more common in younger females + asian ppl

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53
Q

what is first degree heart block

A

delayed conduction through to the AVN.
But every atrial impulse leads to a ventricular contraction (each P wave followed by QRS complex)

PR interval > 0.2 secs

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54
Q

what is second degree heart block

A

some atrial impulses do not make it through the AVN to the ventricles. Instances where P waves not followed by QRS.

2 types: Mobitz type 1 (Wenckebach phenomenon)
Mobitz type 2

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55
Q

what is mobitz type 1 (wenckebach phenomenon)

A

the conduction through the AVN takes progressively longer till it fails + then resets
Increasing PR interval until one is not followed by QRS

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56
Q

what is mobitz type 2

A

failure of conduction through AVN
absence of QRS following P

Usually a set ratio of P waves to QRS complexes. eg 3 P waves for each QRS = 3:1 block

risk of asystole

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57
Q

what is third degree heart block

A

complete heart block.

no observable relationship between P + QRS

signif risk of asystole

can get dizziness, palpitations, syncope

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58
Q

what needs transvenous pacing

A

complete heart block w broad complex QRS

recent asystole

mobitz type 2 block

ventricular pause > 3 secs (PR)

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59
Q

mx of high INR w major bleeding (variceal / IC haemorrhage)

A

stop warfarin
IV VK 5mg AND
Prothrombin complex concentrate

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60
Q

mx of INR>8 w minor bleeding

A

stop warfarin
IV VK 1-3mg
repeat dose VK if still too high after 24 hrs
restart warfarin when INR <5

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61
Q

mx INR > 8 no bleeding

A

stop warfarin
oral VK 1-5mg (IV prep)
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0

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62
Q

INR 5-8 minor bleeding

A

stop warfarin
IV VK 1-3mg
Restart when INR < 5.0

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63
Q

INR 5-8 no bleeding

A

Withhold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose

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64
Q

what anticoag to use w mechanical heart valves

A

warfarin

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65
Q

Examples of fibrinolytic agents (used in thrombolysis in MI)

A

Streptokinase
Alteplase
Tenecteplase

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66
Q

what is dressler’s syndrome

A

also called post-myocardial infarction syndrome.

occurs around 2 – 3 weeks after an acute MI. It is caused by a localised immune response that results in inflammation of the pericardium (pericarditis).

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67
Q

how to dx dressler’s syndrome

A

ECG (global ST elevation and T wave inversion)

echocardiogram (pericardial effusion)

raised inflammatory markers (CRP and ESR).

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68
Q

dressler’s syndrome mx

A

NSAIDs - aspirin/ibuprofen

steroids if severe

Pericardiocentesis?

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69
Q

what do you see on a ECG for LBBB

A

QRS > 120ms
look at v1 - pointing down

W in V1
M in V6

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70
Q

what could new LBBB indicate

A

a new LBBB is always pathological

MI (most likely anterior)
hypertension
aortic stenosis
cardiomyopathy

71
Q

how to prevent further episodes of supraventricular tachy

A

beta-blockers
radio-frequency ablation

72
Q

what to do when a cardiac arrest is witnessed in a monitored patient

A

up to three quick successive (stacked) shocks’, rather than 1 shock followed by CPR

73
Q

medication for stable angina

A

ASPIRIN

STATIN

sublingual GTN to abort attacks

BB or CCB (if in monotherapy use verapamil (CAN’T PRESCRIBE W BB AS HEART BLOCK RISK) / diltiazem)

if poor response increase med to max tolerated dose

if still sx - ADD the one you didn’t use first (CCBs in combo w BB use longer acting like amlodipine, nifedipine)

if can’t tolerate CCB+BB - consider adding:
a long-acting nitrate
ivabradine
nicorandil
ranolazine

74
Q

what drug for wide complex tachycardia

A

amiodarone - loading dose followed by 24 hr infusion

75
Q

what drug for narrow complex tachycardia

A

adenosine

76
Q

what drug for bradycardia

A

atropine

77
Q

when to do an emergency admission for chest pain

A

current chest pain or chest pain in the last 12 hours with an abnormal ECG

78
Q

when to refer for chest pain 12-72 hrs ago

A

refer to hosp for same day assessment

79
Q

when to refer for chest pain > 72 hrs ago

A

perform full assessment w ECG + troponin before deciding on further action

80
Q

most common valve affected in endocarditis

in general
in IVDU

A

in general it is the mitral valve

in IVDU it is the tricuspid valve (first spot blood comes to after general circ)

81
Q

which type of MI may lead to AVN block

A

inferior (occlusion to RCA supplying AVN)

82
Q

what is Wolff-Parkinson White (WPW) syndrome caused by

A

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

83
Q

ecg features of Wolff-Parkinson White (WPW)

A

short PR interval (<120 ms)

wide QRS complexes with a slurred upstroke - ‘DELTA WAVE’

LAD if right-sided accessory pathway

in the majority of cases, or in a question without qualification, Wolff-Parkinson-White syndrome is associated with left axis deviation
RAD if left-sided accessory pathway

84
Q

mx of WPW

A

definitive treatment: radiofrequency ablation of the accessory pathway

medical therapy: sotalol*, amiodarone, flecainide

*avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node - may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation

85
Q

what is the most common valvular defect of rheumatic heart disease

A

mitral stenosis

86
Q

most common cause of mitral stenosis

A

rheumatic fever

87
Q

what is rheumatic fever caused by

A

group A Streptococcus

88
Q

heart sounds in mitral stenosis

A

mid-late diastolic murmur (heard best on expiration)
loud opening snap
then low pitched rumble

89
Q

aortic regurgitation murmur

A

early diastolic murmur
‘austin-flint’ murmur - apex, rumbling
collapsing pulse

90
Q

what is Pulmonary capillary wedge pressure (PCWP)

A

used to assess left ventricular filling, represent left atrial pressure, and assess mitral valve function.

used to differentiate between cardiogenic pulmonary edema and noncardiogenic pulmonary edema
- in cardiac it will be raised

91
Q

what is a pseudoaneurysm

A

the inner two layers (intima + media) rupture and there is dilation of the vessel, with the blood only being contained within the outer (adventitia) layer of the aorta

usually after trauma / surgery

92
Q

RF aortic aneurysm

A

Men are affected significantly more often and at a younger age than women
Increased age
Smoking
Hypertension
Family history
Existing cardiovascular disease
Marfan syndrome and other connective tissue disorders

93
Q

aortic aneurysm presentation

A

Dilation of the thoracic aorta is often asymptomatic

May cause sx due to taking up space within the mediastinum:
Chest/back pain
Trachea/left bronchus compression may cause cough, SOB + stridor
Phrenic nerve compression may cause hiccups
Oesophageal compression may cause dysphagia (difficulty swallowing food)
Recurrent laryngeal nerve compression may cause a hoarse voice

94
Q

ix for aortic aneurysm

A

Echocardiogram
CT or MRI angiogram

95
Q

ma aortic aneurysm

A

treating modifiable risk factors

Surveillance with regular imaging to monitor the size

Thoracic endovascular aortic repair (TEVAR), with a catheter inserted via the femoral artery inserting a stent graft into the affected section of the aorta

Open surgery (midline sternotomy) to remove the section of the aorta with the defect in the wall and replace it with a synthetic graft

96
Q

ruptured aortic aneurysm presentation

A

Severe chest pain or back pain
Haemodynamic instability (hypotension and tachycardia)
Collapse
Death (often patients do not reach hospital)

97
Q

screening for aortic aneurysms

A

single abdominal ultrasound for males aged 65

<3cm nothing
3-4.4cm scan every 12 mths
4.5-5.4cm scan every 3 mths
surgery if >/= 5.5cm

98
Q

Poorly controlled HTN
already taking an ACEi, CCB and a thiazide diuretic
K+ < 4.5
K+ > 4.5

A

add spironolactone

consider bisoprolol

99
Q

HTN patients < 55-years-old or a background of type 2 diabetes mellitus

A

ACE inhibitor or a Angiotensin receptor blocker

100
Q

patients >= 55-years-old or of black African or African–Caribbean origin

A

Calcium channel blocker

101
Q

HTN step 2 tx

A

if already taking an ACE-i/ARB add a CCB or a thiazide-like Diuretic (indapamide)

if already taking a CCB add an ACE-i/ARB or a thiazide-like Diuretic

for patients of black African or African–Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor

102
Q

adv + disadv biological (bioprosthetic) valves

A

Major disadvantage is structural deterioration + calcification over time. Most older patients ( > 65 years for aortic valves and > 70 years for mitral valves) receive a bioprosthetic valve

Long-term anticoagulation not usually needed. Warfarin may be given for the first 3 months depending on patient factors. Low-dose aspirin is given long-term.

103
Q

3rd heart sound

A

dilated cardiomyopathy

104
Q

4th heart sound

A

HOCM

105
Q

pulmonary stenosis murmur

A

ejection systolic murmur louder during inspiration

106
Q

murmur in PDA

A

continuous machinery murmur

107
Q

cardiac output equation

A

CO = SV x HR

108
Q

triggers of acute LEFT ventricular failure

A

often the result of decompensated chronic HF

potential triggers:
iatrogenic (aggressive IV fluids in frail elderly px w impaired LV func)
MI
arrhythmias
sepsis
hypertensive emergency (acute, severe increase in BP)

109
Q

sx acute left ventricular failure

A

acute SOB - exacerbated by lying flat + improves sitting up
will look + feel unwell
cough w frothy white/pink sputum

110
Q

examination acute left ventricular failure

A

raised RR
reduced O2 sats
tachycardia
3rd heart sound
bilateral basal crackles
hypotension in severe cases (cardiogenic shock)

111
Q

what type of resp failure does acute left ventricular failure cause

A

type 1 - low o2 w no raised co2

112
Q

examination findings in right sided HF

A

raised JVP
peripheral oedema

112
Q

assessment in px w acute left ventricular failure

A

ABCDE if acutely unwell
clinical assessment - hx + exam
ECG - ischaemia / arrythmias?
Bloods - anaemia, infection, kidney func, BNP, consider troponin if MI suspected
ABG
CXR
Echo

113
Q

what is the action of BNP

A

released from the heart ventricles when myocardium is stretched beyond normal range
relax the smooth muscle in BVs reducing systemic vascular resistance
also acts as a diuretic to promote water excretion in urine reducing circ vol

114
Q

what is ejection fraction

A

percentage of blood in the left ventricle that is squeezed out with each ventricular contraction. An ejection fraction above 50% is considered normal.

115
Q

how to define cardiomegaly on CXR

A

cardiothoracic ration of > 0.5

116
Q

CXR in acute left ventricular failure

A

upper lobe venous diversion
bilateral pleural effusions
fluid in interlobar fissures (between the lung lobes)
fluid in septal lines (Kerley lines)

117
Q

mx acute left ventricular failure

A

hx admission
if severe pulmonary oedema / cardiogenic shock -> HDU/ICU

S - sit up
O - oxygen
D - diuretics - IV furosemide
I – Intravenous fluids should be stopped
U – Underlying causes need to be identified and treated (e.g. MI)
M – Monitor fluid balance - oral + IV intake monitor, UO, U&Es, body weight

118
Q

what are inotropes

A

meds that alter contractility of the heart
positive inotropes - increase contractility -> increase CO + MAP

119
Q

what are vasopressors

A

meds that cause vasoconstriction increasing systemic vascular resistance + so MAP
can be used to improve BP

120
Q

when would you get HF w preserved ejection fraction

A

ie clinical features of HF but ejection fraction > 50%
it is a result of diastolic dysfunc - issue w LV filling up w blood when relaxing

121
Q

causes of chronic HF

A

ischaemic heart disease
valvular heart disease - commonly aortic stenosis
HTN
arrhythmias - commonly AF
cardiomyopathy

122
Q

presentation of chronic HF

A

breathlessness - worse on exertion
cough - frothy white/pink sputum
orthopnoea
paroxysma nocturnal dyspnoea
peripheral oedema
fatigue

123
Q

examination signs in chronic HF

A

tachycardia
tachypnoea
HTN
murmurs?
3rd heart sound
bilateral basal crackles
raised JVP
peripheral oedema

124
Q

what is paroxysmal nocturnal dyspnoea

A

the experience that px have of suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.

125
Q

establishing dx of chronic HF

A

Clinical assessment (history and examination)
N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test
ECG
Echocardiogram

Other ix include:
Bloods for anaemia, renal function, thyroid function, liver function, lipids and diabetes
Chest x-ray and lung function tests to exclude lung pathology

126
Q

New York Heart Association (NYHA) classification

A

Class I: No limitation on activity
Class II: Comfortable at rest but symptomatic with ordinary activities
Class III: Comfortable at rest but symptomatic with any activity
Class IV: Symptomatic at rest

127
Q

mx chronic HF

A

R – Refer to cardiology
A – Advise them about the condition
M – Medical treatment
P – Procedural or surgical interventions
S – Specialist heart failure MDT input, such as the heart failure specialist nurses, for advice and support

Additional management:
Flu, covid and pneumococcal vaccines
Stop smoking
Optimise treatment of co-morbidities
Written care plan
Cardiac rehabilitation (a personalised exercise programme)

128
Q

what NT-proBNP results mean in regards to referral

A

From 400 – 2000 ng/litre should be seen and have an echocardiogram within 6 weeks
Above 2000 ng/litre should be seen and have an echocardiogram within 2 weeks

129
Q

medical tx for chronic HF

A

A – ACE inhibitor (e.g., ramipril) titrated as high as tolerated (avoid in px w valvular heart dis) (or ARB)
B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated
A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone) (+when there is reduced ejection fraction)
L – Loop diuretics (e.g., furosemide or bumetanide)

130
Q

what murmur can you get with AF

A

mitral stenosis

131
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

132
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

133
Q

mx aortic stenosis

A

if asymptomatic then observe the patient is a general rule
if symptomatic then valve replacement
if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery

134
Q

what is AF

A

where the electrical activity in the atria of the heart becomes disorganised, leading to fibrillation (random muscle twitching) of the atria and an irregularly irregular pulse.

135
Q

overall effects of AF

A

Irregularly irregular ventricular contractions
Tachycardia (fast heart rate)
Heart failure due to impaired filling of the ventricles during diastole
Increased risk of stroke

136
Q

common causes of AF

A

S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I – Ischaemic heart disease
T – Thyrotoxicosis
H – Hypertension

Alcohol and caffeine are lifestyle causes

137
Q

AF presentation

A

Palpitations
Shortness of breath
Dizziness or syncope (loss of consciousness)
Symptoms of associated conditions (e.g., stroke, sepsis or thyrotoxicosis)

138
Q

diff dx for irregularly irregular pulse

A

Atrial fibrillation
Ventricular ectopics

139
Q

how to differentiate between AF + ventricular ectopics

A

Ventricular ectopics disappear when the heart rate gets above a certain threshold. Therefore, a regular heart rate during exercise suggests a diagnosis of ventricular ectopics.

AF will have no P waves on ECG. Ventricular ectopics will

140
Q

what is paroxysmal atrial fibrillation

A

episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm. These episodes can last between 30 seconds and 48 hours.

141
Q

when might you need an echo if you find AF on ECG

A

Valvular heart disease
Heart failure
Planned cardioversion

142
Q

when not to do rate control first line in AF

A

A reversible cause for their AF
New onset atrial fibrillation (within the last 48 hours)
Heart failure caused by atrial fibrillation
Symptoms despite being effectively rate controlled

143
Q

rate control options for AF

A

Beta blocker first-line (e.g., atenolol or bisoprolol)

Calcium-channel blocker (e.g., diltiazem or verapamil) (not preferable in heart failure)

Digoxin (only in sedentary people with persistent atrial fibrillation, requires monitoring and has a risk of toxicity)

144
Q

when to offer rhythm control to px w AF

A

A reversible cause for their AF
New onset atrial fibrillation (within the last 48 hours)
Heart failure caused by atrial fibrillation
Symptoms despite being effectively rate controlled

145
Q

rhythm control options for AF

A

pharm: flecainide, amiodarone (use in structural heart disease)

electrical: cardiac defib

146
Q

when to do immediate cardioversion for AF + how

A

Present for less than 48 hours
Causing life-threatening haemodynamic instability

Can do pharmacological or electrical

147
Q

when to do delayed cardioversion + how

A

present for more than 48 hours and they are stable.

electrical cardioversion is recommended

px should be anticoagulated for at least 3 weeks before delayed cardioversion.

148
Q

long-term rhythm control for AF

A

Beta blockers first-line

Dronedarone second-line for maintaining normal rhythm where patients have had successful cardioversion

Amiodarone is useful in patients with heart failure or left ventricular dysfunction

149
Q

mx paroxysmal atrial fibrillation

A

pill in pocket approach using
FLECAINIDE

use same score for anticoag

150
Q

score to predict risk of stroke in AF + what does that mean for anticoag

A

CHA2DS2-VASc

C = Congestive heart failure 1
H = Hypertension 1
A2 = Age ≥75 years 2
D = Diabetes Mellitus 1
S2 = Prior Stroke/TIA/thromboembolism 2
V = Vascular disease 1
A = Age 65–74 years 1
Sc = Sex category (i.e. female sex) 1

0 = no anticoag
1= consider in men (women automatically score 1)
2+ = offer anticoag

151
Q

score to assess risk of bleeding on anticoag

A

ORBIT

O = Older age ≥75 years
R = Renal impairment (GFR<60)
B = Bleeding previously
I = Iron (low haemoglobin/haematocrit)
T = Taking antiplatelet medication

152
Q

1st line anticoag in AF

A

DOACs - apixaban, endoxaban, rivaroxaban (direct factor Xa inhibitors), Dabigatran (direct thrombin inhibitor).

153
Q

2nd line anticoag in AF

A

warfarin (VK antagonist)

give if advanced CKD

154
Q

criteria for PCI in STEMI

A

ST elevation of >2mm in 2 contiguous chest leads or >1mm in 2 contiguous limb leads

~Chest pain or other evidence of ischaemia

New or presumed new LBBB was an indication for thrombolysis and is
often considered an indication for PPCI in the right clinical context

155
Q

when to measure troponin

A

depends on type of assay
If High-Sensitivity Cardiac Troponin (hs-TnT)
- measure asap
- if raised measure again in 3h - significant rise or fall suggests MI
- if not raised, can rule out MI, unless pain was <6 hrs ago, in which case obtain
further measurement at that point – significant rise suggests MI

  • Does NOT rule out ACS (could still be unstable angina)
  • signif fall after 2 days also dx

(along w clinical features)

156
Q

what happens to troponin levels in MI

A

goes up 3-6 hrs following infarct + peaks at 2 days

157
Q

what is the HEART score

A

Predicts 6-week risk of major adverse cardiac event.

Use when deciding to discharge from ED / admit

0-3 = low risk, dis
4-6 = med risk, obs
7-10 = high risk, obs, tx, CAG

158
Q

mx NSTEMI in ED

A

Aspirin 300mg

Anticoagulation e.g. Fondaparinux 2.5 mg SC - for px who are not at a high risk of bleeding and who are not having angiography/PCI immediately

GRACE score

If for conservative mx:
* Load with P2Y12 inhibitor – TICAGRELOR 180 mg

If for angio(/PCI)
* TICAGRELOR or PRASUGREL 60 mg (not pras if >75, used if having angio)
* Clopidogrel use in ACS 2nd line (if high bleeding risk or already taking oral anticoagulants )

  • Unfractionated heparin
  • Do NOT give beta blocker, ACEi etc. at this stage without specialist supervision (can precipitate cardiogenic shock)
  • IV GTN infusion if ongoing pain

continuous
* Cardiac monitoring >=24 hours
* Mx of comps such as arrhythmia, acute heart failure

159
Q

inpx mx NSTEMI

A
  • Cardiac monitoring >=24 hours
  • Medical vs invasive management
  • PCI vs CABG
  • Commence on secondary prevention
  • Length of stay about 72 hours
  • Monitor for complications
  • Physiotherapy
  • Optimisation of risk factors
160
Q

drugs on TTO for MI

A

Drugs -Big 5
* Aspirin 75 mg OD for life
* Potent P2Y12 inhibitor – ticagrelor 90 mg BD or prasugrel 5-10 mg OD for >=1 year. Can consider a PPI alongside.
* Cardioselective beta blocker (caution if asthmatic, bradycardic, conduction disease) e.g. bisoprolol 2.5 mg OD
* ACEi (/ARB) (caution if hypotensive, severe CKD) e.g. ramipril 2.5 mg OD
* High intensity statin e.g. Atorvastatin 80 mg OD for life
* (PRN GTN)
* Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone) - be v careful if taking w ACEi as both cause hyperkalaemia

161
Q

follow up for MI

A

Follow up
* Clinic 1 month – can consider device therapy if significant LVSD
* Transthoracic echo if not had as inpx
* Cardiac rehabilitation programme
* Smoking cessation
* GP – uptitrate secondary prevention e.g. ramipril and bisoprolol towards 10 mg OD

Advice
* Don’t drive for 1 week if PCI, 4 weeks if no PCI (we advise all px 4 weeks)
* Gradual return to usual activity levels
* Typically 6 weeks off work
* Stop smoking

162
Q

types of MI

A

Type 1: Traditional MI due to an acute coronary event
Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
Type 4: MI associated with procedures such as PCI, coronary stenting and CABG

i.e, “ACDC” mnemonic:
Type 1: A – ACS-type MI
Type 2: C – Can’t cope MI
Type 3: D – Dead by MI
Type 4: C – Caused by us MI

163
Q

ix in anyone with angina

A

Physical examination (e.g., heart sounds, signs of heart failure, blood pressure and BMI)
ECG (a normal ECG does not exclude stable angina)
FBC (anaemia)
U&Es (required before starting an ACE inhibitor and other medications)
LFTs (required before starting statins)
Lipid profile
Thyroid function tests (hypothyroidism or hyperthyroidism)
HbA1C and fasting glucose (diabetes)

Cardiac stress testing

CT coronary angiography GS

Invasive coronary angiography

164
Q

principles of mx for stable angina

A

R – Refer to cardiology
A – Advise them about the diagnosis, management and when to call an ambulance
M – Medical treatment
P – Procedural or surgical interventions
S – Secondary prevention

Referrals are usually sent to the rapid access chest pain clinic (RACPC).

165
Q

non pharm causes for long QT

A

genetic (long QT syndrome)
hypocalcaemia
hypokalaemia
hypomagnesemia

166
Q

normal PR interval

A

120 – 200 ms (0.12-0.20s)

167
Q

causes of RBBB

A

normal variant - more common with increasing age
right ventricular hypertrophy
chronically increased right ventricular pressure - e.g. cor pulmonale
pulmonary embolism
myocardial infarction
atrial septal defect (ostium secundum)
cardiomyopathy or myocarditis

168
Q

drugs that cause long QT

A

Antibiotics: macrolides
Antipsychotics: haloperidol, clozapine
Antidepressants: TCAs
Antiemetics: ondansetron
antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs

169
Q

heart sound in HOCM

A

S4 hit the floor

170
Q

most common cause of S3

A

HF

can be incidental + not signif in young ppl

171
Q

hypothermia ECG

A

j waves

172
Q

mechanism of action of alteplase

A

Activates plasminogen to form plasmin
Plasmin then degrades fibrin, leading to clot dissolution and restoration of blood flow

173
Q

cushing’s triad + when might you get it

A

widening pulse pressure
bradycardia
irregular breathing

a late sign indicating impending brain herniation
Systolic hypertension occurs as a reflex to maintain cerebral perfusion pressure in the presence of raised ICP

finals (27 decks)

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