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
tx of cardiac tamponade
urgent pericardiocentesis (pericardial needle aspiration)
26
classic presentation of myocarditis
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
27
6 ps of acute limb ischaemia
Pulseless Painful Pale Paralysis Paraesthesia Perishingly cold
28
what blood test indicates right ventricular failure
Raised NT‑proBNP
29
causes of pericarditis
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
30
what is pericarditis
inflam of the pericardium (membrane surrounding heart)
31
what is pericardial effusion
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
32
pericarditis presentation
chest pain - sharp, central/anterior, pleuritic, worse when lying down, better when sitting forward low grade fever
33
on auscultation w pericarditis
pericardial friction rub - rubbing scratching sound occurring alongside heart sounds
34
ix for pericarditis
Raised inflam markers -WBCs, CRP, ESR ECG - saddle shaped ST-elevation - PR depression (more specific) Echo to dx pericardial effusion
35
mx pericarditis
NSAIDs - aspirin / ibuprofen colchicine (longer term to reduce recurrence)
36
what is cardiac tamponade (pericardial tamponade)
when the pericardial effusion is large enough to raise the intra-pericardial pressure squeezing the heart. Decreases CO. Emergency needing prompt drainage (pericardiocentesis)
37
what is infective endocarditis
infection of the endocardium (inner surface of the heart). Most commonly affecting heart valves acute, subacute or chronic
38
RFs for endocarditis
IV drug use CKD Immunocompromised Hx of it Structural heart pathology - valvular HD - congenital HD - hypertrophic cardiomyopathy - prosthetic valves - implantable devices
39
most common cause of endocarditis
most common is staph aureus
40
presentation of endocarditis
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
41
endocarditis ix
blood cultures - needed b4 abx 3 blood samples separated by 6 hrs + taken at diff sites ECHO (TOE) - vegetations on valves
42
Dukes criteria for dx endocarditis
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)
43
endocarditis abx + how long
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
44
common cause of sudden cardiac death in young ppl
hypertrophic obstructive cardiomyopathy (HOCM) / left ventricular outflow tract obstruction
45
HOCM inheritance
AD defect in the genes for sarcomere proteins
46
HOCM presentation
mostly asx Non-specific sx - SOB, fatigue, dizzy, syncope, chest pain, palp Severe: sx of HF
47
ix for HOCM
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
48
mx HOCM
- 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
48
what sld be avoided in HOCM activities and meds
Patients are advised to avoid intense exercise, heavy lifting and dehydration. ACE inhibitors and nitrates are avoided as they can worsen the LVOT obstruction.
49
which meds can reduce BNP levels
tx w ACEis ARBs diuretics
50
what can raise BNP
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
51
ix results in left ventricular aneurysm
persistent ST elevation after MI 3rd + 4th heart sound
52
common finding in takayusu's arteritis (a large vessel vasculitis)
absent limb pulse more common in younger females + asian ppl
53
what is first degree heart block
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
54
what is second degree heart block
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
55
what is mobitz type 1 (wenckebach phenomenon)
the conduction through the AVN takes progressively longer till it fails + then resets Increasing PR interval until one is not followed by QRS
56
what is mobitz type 2
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
57
what is third degree heart block
complete heart block. no observable relationship between P + QRS signif risk of asystole can get dizziness, palpitations, syncope
58
what needs transvenous pacing
complete heart block w broad complex QRS recent asystole mobitz type 2 block ventricular pause > 3 secs (PR)
59
mx of high INR w major bleeding (variceal / IC haemorrhage)
stop warfarin IV VK 5mg AND Prothrombin complex concentrate
60
mx of INR>8 w minor bleeding
stop warfarin IV VK 1-3mg repeat dose VK if still too high after 24 hrs restart warfarin when INR <5
61
mx INR > 8 no bleeding
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
62
INR 5-8 minor bleeding
stop warfarin IV VK 1-3mg Restart when INR < 5.0
63
INR 5-8 no bleeding
Withhold 1 or 2 doses of warfarin Reduce subsequent maintenance dose
64
what anticoag to use w mechanical heart valves
warfarin
65
Examples of fibrinolytic agents (used in thrombolysis in MI)
Streptokinase Alteplase Tenecteplase
66
what is dressler's syndrome
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).
67
how to dx dressler's syndrome
ECG (global ST elevation and T wave inversion) echocardiogram (pericardial effusion) raised inflammatory markers (CRP and ESR).
68
dressler's syndrome mx
NSAIDs - aspirin/ibuprofen steroids if severe Pericardiocentesis?
69
what do you see on a ECG for LBBB
QRS > 120ms look at v1 - pointing down W in V1 M in V6
70
what could new LBBB indicate
a new LBBB is always pathological MI (most likely anterior) hypertension aortic stenosis cardiomyopathy
71
how to prevent further episodes of supraventricular tachy
beta-blockers radio-frequency ablation
72
what to do when a cardiac arrest is witnessed in a monitored patient
up to three quick successive (stacked) shocks', rather than 1 shock followed by CPR
73
medication for stable angina
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
what drug for wide complex tachycardia
amiodarone - loading dose followed by 24 hr infusion
75
what drug for narrow complex tachycardia
adenosine
76
what drug for bradycardia
atropine
77
when to do an emergency admission for chest pain
current chest pain or chest pain in the last 12 hours with an abnormal ECG
78
when to refer for chest pain 12-72 hrs ago
refer to hosp for same day assessment
79
when to refer for chest pain > 72 hrs ago
perform full assessment w ECG + troponin before deciding on further action
80
most common valve affected in endocarditis in general in IVDU
in general it is the mitral valve in IVDU it is the tricuspid valve (first spot blood comes to after general circ)
81
which type of MI may lead to AVN block
inferior (occlusion to RCA supplying AVN)
82
what is Wolff-Parkinson White (WPW) syndrome caused by
congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT)
83
ecg features of Wolff-Parkinson White (WPW)
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
mx of WPW
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
what is the most common valvular defect of rheumatic heart disease
mitral stenosis
86
most common cause of mitral stenosis
rheumatic fever
87
what is rheumatic fever caused by
group A Streptococcus
88
heart sounds in mitral stenosis
mid-late diastolic murmur (heard best on expiration) loud opening snap then low pitched rumble
89
aortic regurgitation murmur
early diastolic murmur 'austin-flint' murmur - apex, rumbling collapsing pulse
90
what is Pulmonary capillary wedge pressure (PCWP)
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
what is a pseudoaneurysm
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
RF aortic aneurysm
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
aortic aneurysm presentation
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
ix for aortic aneurysm
Echocardiogram CT or MRI angiogram
95
ma aortic aneurysm
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
ruptured aortic aneurysm presentation
Severe chest pain or back pain Haemodynamic instability (hypotension and tachycardia) Collapse Death (often patients do not reach hospital)
97
screening for aortic aneurysms
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
Poorly controlled HTN already taking an ACEi, CCB and a thiazide diuretic K+ < 4.5 K+ > 4.5
add spironolactone consider bisoprolol
99
HTN patients < 55-years-old or a background of type 2 diabetes mellitus
ACE inhibitor or a Angiotensin receptor blocker
100
patients >= 55-years-old or of black African or African–Caribbean origin
Calcium channel blocker
101
HTN step 2 tx
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
adv + disadv biological (bioprosthetic) valves
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
3rd heart sound
dilated cardiomyopathy
104
4th heart sound
HOCM
105
pulmonary stenosis murmur
ejection systolic murmur louder during inspiration
106
murmur in PDA
continuous machinery murmur
107
cardiac output equation
CO = SV x HR
108
triggers of acute LEFT ventricular failure
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
sx acute left ventricular failure
acute SOB - exacerbated by lying flat + improves sitting up will look + feel unwell cough w frothy white/pink sputum
110
examination acute left ventricular failure
raised RR reduced O2 sats tachycardia 3rd heart sound bilateral basal crackles hypotension in severe cases (cardiogenic shock)
111
what type of resp failure does acute left ventricular failure cause
type 1 - low o2 w no raised co2
112
examination findings in right sided HF
raised JVP peripheral oedema
112
assessment in px w acute left ventricular failure
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
what is the action of BNP
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
what is ejection fraction
percentage of blood in the left ventricle that is squeezed out with each ventricular contraction. An ejection fraction above 50% is considered normal.
115
how to define cardiomegaly on CXR
cardiothoracic ration of > 0.5
116
CXR in acute left ventricular failure
upper lobe venous diversion bilateral pleural effusions fluid in interlobar fissures (between the lung lobes) fluid in septal lines (Kerley lines)
117
mx acute left ventricular failure
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
what are inotropes
meds that alter contractility of the heart positive inotropes - increase contractility -> increase CO + MAP
119
what are vasopressors
meds that cause vasoconstriction increasing systemic vascular resistance + so MAP can be used to improve BP
120
when would you get HF w preserved ejection fraction
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
causes of chronic HF
ischaemic heart disease valvular heart disease - commonly aortic stenosis HTN arrhythmias - commonly AF cardiomyopathy
122
presentation of chronic HF
breathlessness - worse on exertion cough - frothy white/pink sputum orthopnoea paroxysma nocturnal dyspnoea peripheral oedema fatigue
123
examination signs in chronic HF
tachycardia tachypnoea HTN murmurs? 3rd heart sound bilateral basal crackles raised JVP peripheral oedema
124
what is paroxysmal nocturnal dyspnoea
the experience that px have of suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.
125
establishing dx of chronic HF
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
New York Heart Association (NYHA) classification
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
mx chronic HF
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
what NT-proBNP results mean in regards to referral
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
medical tx for chronic HF
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
what murmur can you get with AF
mitral stenosis
131
features of severe aortic stenosis
narrow pulse pressure slow rising pulse delayed ESM soft/absent S2 S4 thrill duration of murmur left ventricular hypertrophy or failure
132
causes of aortic stenosis
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
mx aortic stenosis
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
what is AF
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
overall effects of AF
Irregularly irregular ventricular contractions Tachycardia (fast heart rate) Heart failure due to impaired filling of the ventricles during diastole Increased risk of stroke
136
common causes of AF
S – Sepsis M – Mitral valve pathology (stenosis or regurgitation) I – Ischaemic heart disease T – Thyrotoxicosis H – Hypertension Alcohol and caffeine are lifestyle causes
137
AF presentation
Palpitations Shortness of breath Dizziness or syncope (loss of consciousness) Symptoms of associated conditions (e.g., stroke, sepsis or thyrotoxicosis)
138
diff dx for irregularly irregular pulse
Atrial fibrillation Ventricular ectopics
139
how to differentiate between AF + ventricular ectopics
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
what is paroxysmal atrial fibrillation
episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm. These episodes can last between 30 seconds and 48 hours.
141
when might you need an echo if you find AF on ECG
Valvular heart disease Heart failure Planned cardioversion
142
when not to do rate control first line in AF
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
rate control options for AF
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
when to offer rhythm control to px w AF
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
rhythm control options for AF
pharm: flecainide, amiodarone (use in structural heart disease) electrical: cardiac defib
146
when to do immediate cardioversion for AF + how
Present for less than 48 hours Causing life-threatening haemodynamic instability Can do pharmacological or electrical
147
when to do delayed cardioversion + how
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
long-term rhythm control for AF
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
mx paroxysmal atrial fibrillation
pill in pocket approach using FLECAINIDE use same score for anticoag
150
score to predict risk of stroke in AF + what does that mean for anticoag
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
score to assess risk of bleeding on anticoag
ORBIT O = Older age ≥75 years R = Renal impairment (GFR<60) B = Bleeding previously I = Iron (low haemoglobin/haematocrit) T = Taking antiplatelet medication
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1st line anticoag in AF
DOACs - apixaban, endoxaban, rivaroxaban (direct factor Xa inhibitors), Dabigatran (direct thrombin inhibitor).
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2nd line anticoag in AF
warfarin (VK antagonist) give if advanced CKD
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criteria for PCI in STEMI
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
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when to measure troponin
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)
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what happens to troponin levels in MI
goes up 3-6 hrs following infarct + peaks at 2 days
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what is the HEART score
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
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mx NSTEMI in ED
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
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inpx mx NSTEMI
* 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
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drugs on TTO for MI
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
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follow up for MI
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
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types of MI
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
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ix in anyone with angina
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
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principles of mx for stable angina
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).
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non pharm causes for long QT
genetic (long QT syndrome) hypocalcaemia hypokalaemia hypomagnesemia
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normal PR interval
120 – 200 ms (0.12-0.20s)
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causes of RBBB
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
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drugs that cause long QT
Antibiotics: macrolides Antipsychotics: haloperidol, clozapine Antidepressants: TCAs Antiemetics: ondansetron antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs
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heart sound in HOCM
S4 hit the floor
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most common cause of S3
HF can be incidental + not signif in young ppl
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hypothermia ECG
j waves
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mechanism of action of alteplase
Activates plasminogen to form plasmin Plasmin then degrades fibrin, leading to clot dissolution and restoration of blood flow
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cushing's triad + when might you get it
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