cardiovascular conditions Flashcards
(247 cards)
1
Q
subarachnoid haemorrhage presentation
A
thunderclap headache, very high intensity, may have had an episode of a sentinel headache: leading up to event less intense one, meningism: photophobia and neck stiffness
nausea and vomiting
can also have ECG changes such as ST elevation
2
Q
most common cause of subarachnoid haemorrhage
A
trauma
otherwise its spontaneous
3
Q
most common pathophysiology of spontaneous subarachnoid haemorrhage
A
berry aneurism
4
Q
condiitons associated with berry aneurism
A
polycystic kidney disease
5
Q
conditions associated with spontaneous sub haem
A
cardiovscular disease such as ehlers danlos syndrome and coarctation of the aorta
6
Q
first line investigation for subarachnoid haemorrhage
A
non contrast ct head
7
Q
if CT is normal?
A
if done within 6 h of symptom onset then NO LP and you trust the CT
if more than 6 hours after you need to do a lumbar puncture
8
Q
how many hours after symptom onset can you preform LP?
A
AT LEAST 12 HOURS After
to allow the development of xanthochromia (the result of red blood cell breakdown).
xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure).
9
Q
what finding other than xanthochromia is characteristic of Subarach haem on LP?
A
NORMAL or raised opening pressure
10
Q
next steps after identifying subarach ahem on non contrast ct?
A
referral urgent to neuro
CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM (arterovenous malformation)
+/- digital subtraction angiogram (catheter angiogram)
11
Q
management of subarachnoid haemorrhage
A
1) supportive
bed rest
analgesia
venous thromboembolism prophylaxis
discontinuation of antithrombotics (reversal of anticoagulation if present)
2) vasospasm is prevented using a course of oral nimodipine
3) !!!!definitive!!!! intracranial aneurysms are at risk of rebleeding and therefore require prompt intervention, preferably within 24 hours
most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon
12
Q
complications of subarachnpoid haem
A
re-bleeding
happens in around 10% of cases and most common in the first 12 hours
if rebleeding is suspected (e.g. sudden worsening of neurological symptoms) then a repeat CT should be arranged
associated with a high mortality (up to 70%)
hydrocephalus
hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculoperitoneal shunt
vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
ensure euvolaemia (normal blood volume)
consider treatment with a vasopressor if symptoms persist
hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
seizures
13
Q
Important predictive factors in SAH:
for prognosis
A
conscious level on admission
age
amount of blood visible on CT head
14
Q
cardiac tamponade presentation
A
becks triad- hypotension, raised jvp, muffled heart sounds
(think- 1 thing before heart picks up blood, one thing while heart holds blood, one thing after it sends it away)
15
Q
other features of cardiac tamponade
A
dyspnoea, tachycardia, pulsus paradoxus- frop in bp during inspiration!!! important differentiator to restrictive pericarditis
ecg: electrical alternans: when QRS complex alternates form tall to short ect.
16
Q
cardiac tamponade management
A
urgent pericardiocentesis
17
Q
anaphylaxis DEFINING features
A
ABC features SO
airway (throat and tongue swelling)
and/OR breathing (wheeze and dyspnoea)
and/OR circulation problems (hypotensive, tachycardic)
18
Q
additional possible anaphylaxis symptoms
A
generalised pruritus
widespread erythematous or urticarial rash
19
Q
adrenaline dose used for dif ages
A
under 6 months 100-150 microoog
6mo-6y 150 μg
6-12 y 300 μg
500 microog over 12 yrs
20
Q
after how long can you repeat IM Adrenaline if needed
A
5 mins
21
Q
anaphylaxis management after stabilisation
A
1) non sedating oral antihistamines
2) serum tryptase taken to confirm anaphylaxis when unsure since can remain high up to 12 h after
3) new diagnosis: allergy clinic referral
4) adrenaline injector 2 autoinjectors given
22
Q
discharge approach for anaphylaxis
A
2 hours post symptoms resolution in best case scenario
6 h minimum if 2 doses of adrenaline needed or PREVIOUS biphasic reaction
12h minimum if
> 2 doses req
severe asthma
possible ongoing reaction (slow release meds)
late night
difficult emergency access
23
Q
what is refractory anaphylaxis
A
when doesnt resolve after 2 IM adrenaline
iv fluids given for shock
specialist help to consider IV adrenaline
24
Q
most common causes of anaphylaxis
A
food
drug
venom
25
how to categorise tachyarrhythmias
1) SUPRAVENTRICULAR arrhythmias and ventricular
2) supraventricular arrhythmias: AF (the only irregularly irregular arrhythmia), SVTs: regularly irregular, Atrial flutter, WPW syndrome
3) ventricular: monomorphic VT, polymorphic VT, ventricular fibrillation
26
which is the most common sustained (it stays and you have it all the time) arrhythmia?
AF
27
AF pathophysiology
the atria depolarise spontaneously in a RAPID and UNCOORDINATED fashion often > 300bpm and the AV node filters this and so some beat signals are passed on to ventricles but not with any pattern so ventricular beat usually falls< 200 so around 100-150 but is IRREGULARLY IRREGULAR
28
classification of AF
Paroxysmal AF - When it terminates spontaneously or due to intervention within 7 DAYS
Presistent AF when mosre than 7 days
permanent AF- when its accepted to be permanent and no further attempts to restore sinus rhythm are made
29
ECG findings of AF
missing P waves and irregularly irregular rhythm and tachycardic
30
clinical presentaton of AF
non specific can have many forms
-fast irregular palpitations of "cardiac nature" (meaning defined onset, duration and offset)
- effort intolerance ect sometimes only recognised after treated
- sometimes present with stroke
- syncope rare (more a bradyarrhythmia thing)
- congestive heart failure
- asymptomatic and only picked up from heart rate
31
management principles of AF
anticoagulation (arguably most important)
rate control
rhythm control
32
when is anticoagulation considered in AF
for all types, even if paroxismal bla bla ALWAYS!
33
How to assess if someone needs anti coagulation in AF?
CHA2DS2-VASc score
34
what are the categories in CHA2DS2-VASc score
congestive heart failure
hypertension
age>/= 75 (And age 65-74 is 11 point)
diabetes
prior Stroke TIA or Thromboembolism (2 point)
VAscular history
sex female- 1
35
what is the anticoagulation strategy based on the chadvasc score?
0 No treatment
1 Males: Consider anticoagulation
Females: No treatment (this is because their score of 1 is only reached due to their gender)
2 or more Offer anticoagulation
36
what do you need to ensure if chadvasc score suggests no anticoagulatoin is required?
transthoracic echo has been done to exclude valvular disease which in combo with af would be absolute INDICATION for anticoagulatio
37
what is the scoring system used to assess bleeding risk for people receIving anticoagulation for AF
ORBIT score
38
list orbit score criteria
Haemoglobin <130 g/L for males and < 120 g/L for females, or haemtocrit < 40% for males and < 36% for females 2
Age > 74 years 1
Bleeding history (GI bleeding, intracranial bleeding or haemorrhagic stroke) 2
Renal impairment (GFR < 60 mL/min/1.73m2) 1
Treatment with antiplatelet agents 1
39
what is the classification of bleeding risk based on ORBIT score?
ORBIT score Risk group Bleeds per 100 patient-years
0-2 Low 2.4 (bleeds per 10 pt years)
3 Medium 4.7
4-7 High 8.1
40
first and second line anticoagulants used for AF
DOACS first
warfarrin second for ex in someone with prosthetic valve or other contraindic of doac
41
rate/ rhythm management of someone presenting with AF that is haemodynamically unstable
electrical cardioversion
42
rate/ rhythm management of someone presenting with AF that is haemodynamically stable
if <48 hours rhythm control
if >48 hours or uncertain rate control
43
what needs to be ensured if patient considered for long-term rhythm control
ensure anticoagulated for min 3 weeks
44
rate control drugs
beta blocker
calcium channel blocker
digoxin
45
important contraindication for beta blocker?
asthma
46
rhythm control drugs
beta blockers
dronedarone: second-line in patients following cardioversion
amiodarone: particularly if coexisting heart failure
47
when is catheter ablation used in AF
for those with AF who have not responded to or wish to avoid, antiarrhythmic medication.
48
anticoagulation after catheter ablation in AF
should be used 4 weeks before and during the procedure
it should be remember that catheter ablation controls the rhythm but does not reduce the stroke risk, even if patients remain in sinus rhythm. Therefore, patients still require anticoagulation as per their CHA2DS2-VASc score
if score = 0: 2 months anticoagulation recommended
if score > 1: longterm anticoagulation recommended
49
catheter ablation outcome
notable complications include
cardiac tamponade
stroke
pulmonary vein stenosis
success rate
around 50% of patients experience an early recurrence (within 3 months) of AF that often resolves spontaneously
longer term, after 3 years, around 55% of patients who've had a single procedure remain in sinus rhythm. Of patients who've undergone multiple procedures around 80% are in sinus rhythm
50
SVT pathogenesis
its re-entrant circuit due to an additional electrical oathway
1) AVNRT
2) AVRT
51
ecg diagnosis of SVT
reggularly irregular,
present p waves abnormally shaped
150-200bpm
NARROW COMPLEX
52
treatment of SVT
1) vagal manoeuvres
2) drugs: adenosine rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18
53
what is contraindication of IV adenosine and alternative used?
contraindicated in asthmatics - verapamil is a preferable option
54
last resort of SVT treatment
electrical cardioversion
55
A flutter characteristics
saw tooth
atrial depol occur 300bpm and conduction to ventricles is limmited to every decond, third or fourth dep, most commonly 2nd so hr is exact 150 bpm
may be asymtomatic or breathless and palpitations and can occur with AF commonly
56
atrial flutter treat
radiofreq ablation is safe and good success
57
types of ventricular tachycardias
monomorphic
polymorphic
ventricular fibrillation
58
important suvbtype of POLYMORPHIC VT and what triggers it?
torsades des pointes triggered by QT prolongation
59
cAUSES of prolonged QT
Congenital:
Jervell-Lange-Nielsen syndrome (includes deafness
Romano-Ward syndrome (no deafness)
DRUGS:
amiodarone, sotalol, class 1a antiarrhythmics
tricyclic antidepressants, fluoxetine
chloroquine
terfenadine
erythromycin
OTHER:
electrolyte:
HYPO
K+
CA2+
Mg2+
-acute myocardial infarction
-myocarditis
-hypothermia
-subarachnoid haemorrhage
60
WHEN do you use DC cardioversion in VTs?
when adverse signs: systolic BP < 90 mmHg, chest pain, heart failure
and if none of these signs but drugs (Antiarrhythmics) were given failed
61
antiarrhytmic drugs used in VT
amiodarone: ideally administered through a central line
lidocaine: use with caution in severe left ventricular impairment
procainamide
62
WHAT ELSE is done in the case that antiarrhythmics fail as a maintnance therapy in VT?
If drug therapy fails
electrophysiological study (EPS)
implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function
63
what drug cant be given as antiarrhytmhic in VT
VERAPAMIL
64
what condition does the exam buzzword "pink frothy sputum" point to?
heart failure
65
what are the 3 classifications of peripheral arterial disease
1) intermittent claudication
2) critical limb ischemia
3) acute limb threatening ischemia
66
presentation of intermittent claudication
- aching or burning in the leg muscles following walking
- patients can typically walk for a predictable distance before the symptoms start
- usually relieved within minutes of stopping
- not present at rest
67
Assessment for intermittent claudication (investigations)
check pulses (femoral, popliteal, posterior tibialis and dorsalis pedis)
check ABPI
duplex ultrasound is first line investigation
magnetic resonance angiography (MRA) should be performed prior to any intervention
68
treatment for peripheral arterial disease
statin and clopidogrel
and a supervised EXERCISE program: exercise training
69
treatment options of critical limb ischemia or severe PAD
endovascular revascularisation (for <10 cm aortic iliac disease and high risk patients
surgical revascularisation: > 10 cm lesions, multifocal, lesions of the common femoral artery and purely infrapopliteal disease
70
diagnosis of critical limb ischemia
if theres one or more of the following features:
- rest pain (also over night/ when sleeping) in foot for more than 2 weeks
- ulceration (tissue death)
- gangrene
ABPI: <0.5
(patients often report sleeping with legs hanging of bed to aleviate pain)
71
presentation of acute limb ischaemia time frame vs chronic
<2 weeks
72
acute limb threatening ischaemia features
one or more of the 5P+C
PULSELESS
painful
paralysed
pale
paraesthetic
COLD
73
acute limb threatening ischaemia initial investigations
handheld arterial Doppler examination
if doppler signals are present then you do an ABPI to check
74
ABPI Normal valies and mild moderate severe limb ischaemia
>1.2 if calcified its non compressible ( seen in diabetes)
0.9-1.2 normal
0.7-0.9 is minimal symptoms - mild limb ischaemia
0.7-0.4 moderate - claudication
<0.4 severe limb ischaemia - critical leg ischaemia
75
what is leriche syndrome
buttock claudication
impotence
reduced pulses
76
once acute limb- threatening ischaemia is confirmed what aspect is it also good to establish?
whether its caused by a thrombus or an embolus
an embolus doesnt have any previous pain in leg or difficulties in past and also more unilateral and no vascular disease
maybe indication of a clear cause eg AF tips you towards that for sure
77
initial management of acute limb threatening ischaemia presentation
ABC approach
analgesia : IV opioids often used
IV unfractioned heparin - prevent thrombus propagation especially if patient not suitable for immediate surgery
vascular review
78
definitive management of acute limb threatening ischaemia
intra arterial thrombolysis
surgical embolectomy
angioplasty
bypass surgery
amputation if irreversible (if more than 6-10 hours after onset)
79
what is endarterectomy
removing the calcification in any artery that is clogge and putting in a smth to keep it wide and open
80
WHEN Are endovascular revascularization techniques used over surgical revascularization?
endovascular techniques are typically used for short segment stenosis (e.g. < 10 cm), aortic iliac disease and high-risk patients
81
how to organise the types of peripheral venous disease
1) the disease that causes progressive venous problems and incompetence is termed:
chronic venous insufficiency - this can be in deep or superficial veins with dif problems in each
2) classification system for progression of venous disease: CEAP classification based on clinical presentation of the disease
3) think about different pathologies in DEEP vein insufficiency and superficial vein insufficiency
82
presentation of varicose veins (SYMptoms)
itchyness, painful, swollen, can feel heavy, burning or throbbing pain
83
risk factors of varicose veins
old age , prolonged immobility or standing still for long, obesity, female!, pregnant!
84
management of varicose veins
most cases dont require surgery just compression stockings and putting feet up when resting ect
weight loss
exercise
85
when is surgery indicated for varicose veins?
when theres significant symptoms or some form of complication: ulcer (HEALED or active) , bleeding, superficial thrombophlebitis, skin change (pigmentation or eczema)
86
what are the possible invasive treatment options of varicose veins
endothermal ablation: using either radiofrequency ablation or endovenous laser treatment
foam sclerotherapy: irritant foam → inflammatory response → closure of the vein
surgery: either ligation or stripping
87
abdominal aortic aneurism presentation
USUALLY asymptomatic!!!
if there are symptoms its non specific abdo pain or expansile mass on examination with both hands ect
88
aneurism definition
localised dilation of >50% of normal diameter of a blood vessel which involves all layers
89
screening for AAA
males when they turn 65! single abdominal ultrasound
90
screening classifications based on size of AAA
< 3cm normal and no further action
3-4.4 small 0 rescan yearly
4.5-5.4- medium rescan every 3 months
for small and medium also minimise cardiovascular risk factors
>/= 5.5 is large OR
if rapidly enlarging: > 1cm / year (regardless of actual size)
refer urgently (2 weeks) to vascular surgery for probable intervention
91
presentation of RUPTURED abdominal aortic aneurism
severe, central abdominal pain radiating to the back
pulsatile, expansile mass in the abdomen
patients may be shocked (hypotension, tachycardic) or MAY HAVE COLLAPSED
92
MANAGEMENT OF ruptured AAA
IMMEDIATE vascular review with a view to emergency repair
in haemodynamically unstable patients no CT straight to theatres
if frail consider paliative as they may die either way
haemodynamically stable may be sent for CT angio where diagnosis in doubt - also to assess the suitability of endovascular repair
93
most common site of venous ulceration
above the medial malleolus- in gaiter area of leg: aka: between ankle and mid calf
94
investigations to do if a venous ucer is not healing
ankle-brachial pressure index (ABPI) is important in non-healing ulcers to assess for poor arterial flow which could impair healing
95
what is an abnormal ABPI and what does it indicate
a 'normal' ABPI may be regarded as between 0.9 - 1.2. Values below 0.9 indicate arterial disease.
96
in what case could someone hace an ABPI >1.3 ?
values above 1.3 may also indicate arterial disease, in the form of false-negative results secondary to arterial calcification (e.g. In diabetics)
97
management of venous ulceration
compression bandaging, usually four layer (only treatment shown to be of real benefit)
oral pentoxifylline, a peripheral vasodilator, improves healing rate
98
what elements do you need to check when examining an ulcer
- Location
* Size
* Shape
* Depth
* Edge
* Base
* Signs of infection–
redness/discharge
99
arterial ulcer presentation
very painful
well demarcated
deep
on sites of pressure commonly!! more LATERAL maleoli and toes or heels
100
investigations for arterial ulcer
diagnosis usually clinical but to confirm you do
Ankle-brachial pressure index (ABPI): An ABPI less than 0.9 suggests peripheral arterial disease.
Doppler ultrasound: Doppler ultrasound is used to assess blood flow and identify any blockages or narrowing in the arteries.
101
management of arterial ulcers
Consider referral for angiography or duplex ultrasound if ABPI is less than 0.8 or if there are signs of severe ischaemia.
Endovascular procedures or bypass surgery may be necessary based on the severity of peripheral artery disease.
wound care
pain management
lifestyle (cardio rf)
102
dry vs wet gangrene compare and contrast
1) cause + progression: dry is by chronic ischaemia due to PAD - sloww progression
vs wet is sudden lack of blood supply combined with bacterial infection - fast progression and can lead to systemic sepsis
2) Appearance: dry shrivelled and blackened + clear demarcation between necrotic and healthy
VS swolen, moist, blistered tissue with foul odour
3) pain: painless in dry and painful in wet
103
what is gas gangrene
Caused by infection with Clostridium bacteria, which produce gas and toxins.
104
gas gangrene presentation
Severe pain and swelling at the site of infection.
Crepitus due to gas production by Clostridium bacteria.
Rapid onset of systemic symptoms, including tachycardia, hypotension, and shock.
105
what is necrotising fascitis
A severe form of gangrene involving the fascia and subcutaneous tissues.
Caused by mixed bacterial infections, often including Streptococcus pyogenes and Staphylococcus aureus.
106
necrotising fasciitis presentation
Intense pain disproportionate to the visible signs.
Rapid progression of erythema, swelling, and tissue necrosis.
Systemic signs of sepsis, such as fever, tachycardia, and hypotension
107
management of gangrene principles
control infection
restore blood supply
remove necrotic tissue
108
surgical interventions in gangrene
Debridement: Surgical removal of necrotic tissue to prevent the spread of infection.
Amputation: In severe cases, partial or complete amputation of the affected limb may be necessary.
Revascularisation: Procedures such as angioplasty or bypass surgery to restore blood flow in cases of arterial occlusion.
109
antibiotics when needed in gangrene what are they
Empirical broad-spectrum antibiotics initially, followed by targeted therapy based on culture results.
For gas gangrene, high-dose penicillin and clindamycin are often recommended.
110
what is another thing used in some cases of gas gangrene
Hyperbaric oxygen therapy:
Used in some cases of gas gangrene to enhance oxygen delivery to ischaemic tissues and inhibit anaerobic bacterial growth.
111
what are the clinical features outlined in two level DVT wells score
risk factor related:
- active cancer
- paralysis paresis or recent plaster
immobilisation of lower extremities
- recently bedridden for >3 d or major
surgery requiring any anaesthesia
- previously documented DVT
Symptom related
- localised tenderness along the distribution of the deep venous system
- entire leg swollen
- calf swelling >3cm larger than normal leg
- pitting oedema only on symptomatic leg
- collateral superficial veins (non varicose)
alternative diagnosis equally likely is -2 points
112
clinical probability definition based on wells score
>/= 2 likely
1 or less unlikely
113
what is done if wells>/=2
a proximal leg vein ultrasound needs to be done
114
what is don if wells
D DIMER
115
what happens if any of the needed investigations cant be done within 4 hours in DVT
give interim anticoagulation
116
what happens if negative proximal leg vein US?
need to do d dimer, if thats positive:
repeat scan in 6-8 days and stop anticoagulation
117
what if wells <1 and dvt positive
you do proximal leg vein us scan
118
how should blood be obtained for d dimer
recommend either a point-of-care (finger prick) or laboratory-based test
119
d dimer cut offs used
age-adjusted cut-offs should be used for patients > 50 years old
120
management of confirmed dvt
DOAC even for cancer patientss
121
who doesnt get doac in DVT management?
if renal impairment is severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA
if the patient has antiphospholipid syndrome (specifically 'triple positive' in the guidance) then LMWH followed by a VKA should be used
122
length of anticoagulation
3 months if provoked (maybe 3-6 if active cancer)
6 months if unprovoked
123
what is the definition of cardiac arrest
cessation of functional circulation due to failure in the heart's pumping action.
can be categorised as asystole, pulseless electrical activity (PEA), ventricular fibrillation (VF) or pulseless ventricular tachycardia (pVT)
124
causes of cardiac arrest
4H
4T
hypovolaemia
hypothermia
hypoxia
hypokalaemia + hyper, hypocalcaemia and hyper - ph abnormal and other metabolic imbalances
Thrombosis (coronary or pulmonary) , tamponade, toxins, tension pneumothorax
125
management principles of cardiac arrest
'shockable' rhythms: ventricular fibrillation/pulseless ventricular tachycardia (VF/pulseless VT)
'non-shockable' rhythms: asystole/pulseless-electrical activity (asystole/PEA)
in all cases ALS - 30:2
126
non shockable rhythms
adrenaline 1 mg as soon as possible for non-shockable rhythms]
repeat adrenaline 1mg every 3-5 minutes whilst ALS continues
127
what is done in shockable rhythms eg VF/pulseless VT
a single shock for VF/pulseless VT followed by 2 minutes of CPR
if the cardiac arrested is witnessed in a monitored patient (e.g. in a coronary care unit) then the 2015 guidelines recommend 'up to three quick successive (stacked) shocks', rather than 1 shock followed by CPR
during a VF/VT cardiac arrest, adrenaline 1 mg be given once chest compressions have restarted after the third shock
+
amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered.
a further dose of amiodarone 150 mg should be given to patients who are in VF/pulseless VT after 5 shocks have been administered
lidocaine used as an alternative if amiodarone is not available or a local decision has been made to use lidocaine instead
128
what to do if suspecting a PE as the cause of cardiac arrest
should be considered if a pulmonary embolus is suspected
if given, CPR should be continued for an extended period of 60-90 minutes
129
how should drugs be delivered during cardiac arrest
IV access should be attempted and is first-line
if IV access cannot be achieved then drugs should be given via the intraosseous route (IO)
130
what is acute pericarditis
inflammation of the pericardial sac lasting less than 4-6 weeks
131
infectious causes of acute pericarditis
viral infections (Coxsackie)
tuberculosis
132
non infectious causes of acute pericarditis
uraemia
post-myocardial infarction
early (1-3 days): fibrinous pericarditis
late (weeks to months): autoimmune pericarditis (Dressler's syndrome)
radiotherapy
connective tissue disease:
systemic lupus erythematosus
rheumatoid arthritis
hypothyroidism
malignancy:
lung cancer
breast cancer
trauma
133
features of acute pericarditis
chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include a non-productive cough, dyspnoea and flu-like symptoms
pericardial rub
134
investigations done for acute pericarditis
ECG
transthoracic echo
bloods
135
ECG changes seen in acute pericarditis
global/ widespread as opposed to territories seen in ischaemic events
saddle shaped ST elevation
PR depression: MOST SPECIFIC ECG marker for pericarditis: think PR PERI LOW
136
blood test findings of acute pericarditis
inflammatory markers
TROPONIN - around 30% of patients may have leevatef- this indicates possible myopericarditis
137
is management of acute pericarditis done as an inpatient or outpatient
the majority of patients can be managed as outpatients
patients who have high-risk features such as fever > 38°C or elevated troponin should be managed as an inpatient
138
first line management for patients with acute idiopathic or viral pericarditis? and how long
a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis
therapy is continued until symptom resolution and normalisation of inflammatory markers (usually 1–2 weeks), followed by a taper of the dose over a further 2–4 weeks
139
other important principles in management of acute pericarditis
strenuous physical activity should be avoided until symptom resolution and normalisation of inflammatory markers
athletes should avoid strenuous exercise for at least 3 months until symptoms have resolved and investigations (CRP, ECG, and echocardiography) have normalised
(and treat underlying cause if something requiring specific treatment eg cancer hypothyroidism ect)
140
what are the causes of constrictive pericarditis
any cause of pericarditis
particularly TB
141
presentation of constrictive pericarditis
dyspnoea
right heart failure: elevated JVP, ascites, oedema, hepatomegaly
JVP shows prominent x and y descent
pericardial knock - loud S3
Kussmaul's sign is positive-- jvp rise with inspiration
142
what is an investigation done for constrictive pericarditis and what does it show
pericardial calcification shown on CXR
143
what is cardiac tamponade
accumulation of pericardial fluid under pressure
144
classic symptom triad of cardiac tamponade
Beck's triad: HYPOTENSION, raised JVP, muffled heart sounds
145
other features of cardiac tamponade
DYSPNOEA
tachycardia
pulsus paradoxus
ECG electrical alternans!!!!
146
management of cardiac tamponade
urgent pericardioscentesis
147
what is an important differential for a younger patient presenting with central chest pain and ST elevation?
myocarditis! can have these features
148
what is myocarditis and who is it more common in
Myocarditis describes inflammation of the myocardium. There are a wide range of underlying causes. It should be particularly considered in younger patients who present with chest pain.
149
causes of myocarditis
viral: coxsackie B, HIV
bacteria: diphtheria, clostridia
spirochaetes: Lyme disease
protozoa: Chagas' disease, toxoplasmosis
autoimmune
drugs: doxorubicin
150
presentation of myocarditids
usually young patient with an acute history
chest pain
dyspnoea
arrhythmias
151
investigations important for myocarditis
bloods: inflammatory markers, cardiac enzymes, BNP (all these will be elevated) and ECG
152
ECG findings of myocarditis
tachycardia
arrhythmias
dyspnoea
153
management of myocarditis
treatment of underlying cause e.g. antibiotics if bacterial cause
supportive treatment e.g. of heart failure or arrhythmias
154
complications of myocarditis
heart failure
arrhythmia, possibly leading to sudden death
dilated cardiomyopathy: usually a late complication
155
ECG findings of hypokalemia
prolonged PR interval
prolonged QT
U waves
small or absent T waves
ST depression
156
ecg findings of hyperkalaemia
peaked T waves
loss of p waves
broad QRS complexes
Sinusoidal wave pattern
v fib
157
hypercalcaemia ecg findings
short QT -- κοντο = κιουτιΚΑ ΑΣ ΙΝ καλσιουμ
158
hypocalcaemia ecg findings
long QT
159
what is the definition of angina
Angina pectoris is chest pain or discomfort caused by transient myocardial ischaemia – when oxygen demand of the heart temporarily exceeds supply, typically due to coronary artery disease (CAD).
160
distinguish between stable and unstable angina
Stable angina = predictable, exertion-induced, no acute plaque rupture.
Unstable angina = unpredictable, progressively worse: eg. at rest or worsening on exertion, likely due to plaque instability and thrombus formation.
161
162
what features define anginal pain in a patient presenting with chest pain
1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
2. precipitated by physical exertion
3. relieved by rest or GTN in about 5 minutes
patients with all 3 features have typical angina
patients with 2 of the above features have atypical angina
patients with 1 or none of the above features have non-anginal chest pain
163
what is the distinction between unstable angina and NSTEMI
main difference is whether troponin is raised in NSTEMI vs not in unstable angina
troponin indicates the death of myocardial cells so in NSTEMI some INFARCTION (cell death blabla) has occurred vs NOT in unstable angina
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which conditions are classified under ACS
STEMI
NSTEMI
unstable angina
165
what is the next step after initial management of an ACS (investigations)
determining if its a STEMI, Nstemi or unstable angina
ECG - applying STEMI criteria to see if its present
troponin
166
what are the ECG and time criteria for a STEMI
clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
---2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
---1.5 mm ST elevation in V2-3 in women
---1 mm ST elevation in other leads
---new LBBB (LBBB should be considered new unless there is evidence otherwise)
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what is the first step after a STEMI has been confirmed
assess eligibility for coronary reperfusion therapy:
PERCUTANEOUS coronary intervention
or
fibrinolysis
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when should a PCI be done
if the presentation is within *12 hours of the onset of symptoms
AND
PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (ie when they were assessed in hospital)
*if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered
169
when is fibrinolysis offered
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
170
if a patient is going to have a PCI what other steps need to be taken prior
Further antiplatelet prior to PCI
this is termed '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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drug therapy during PCI with radial access
unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus
172
drug therapy during PCI with femoral access
bivalirudin with bailout GPI
173
what other medication should patients undergoinf fibrinolysis be given
Patients undergoing fibrinolysis should also be given an antithrombin drug.
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how long after fibrinolysis should ECG be repeated and when should pci be considered
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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what are the two management options for NSTEMI/ unstable angina and how is one chosen?
conservative management
PCI
It's determined by risk assessing patients using tools such as: GRACE tool: Global Registry of Acute Coronary Events
- most widely used tool
176
what factors are taken into account in the GRACE risk assessment tool?
age
heart rate, blood pressure
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels
177
over what predicted 6 month mortality % is PCI suggested for NSTEMI and unstable angina patients
> 3%: intermediate/ high risk
<3%: low risk
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Which patients with NSTEMI/unstable angina should have coronary angiography (with follow-on PCI if necessary)?
--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
179
conservative management of NSTEMI/ unstable angina
Further drug therapy
- further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug)
--- if the patient is not at a high risk of bleeding: ticagrelor
--- if the patient is at a high risk of bleeding: clopidogrel
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types of heart failure
acute/ chronic
left/ right
reduced ejection fraction (mostly "systolic" HF) / preserved ejection fracture (mostly diastolic)
other types: high output, caused by abnormally INCREASED body metabolic demand despite normal heart (eg anemia ect)
181
what is cor pulmonale
it is right sided heart failure caused by respiratory disease!!!
182
what is considered a reduced ejection fraction and what proportion of HF patients have that type of HF
measured using echocardiography: reduced LVEF < 35 to 40%.
This is termed heart failure with reduced ejection fraction (HF-rEF) and affects roughly 50% of people diagnosed with heart failure.
183
causes of HF associated with systolic dysfinction
Ischaemic heart disease
Dilated cardiomyopathy
Myocarditis
Arrhythmias
184
causes of HF associated with diastolic dysfunction
Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis
185
left HF symptoms
pulmonary oedema:
-dyspnoea
-orthopnoea
-paroxysmal nocturnal dyspnoea
-bibasal fine crackles
186
right HF symptoms
- peripheral oedema
---ankle/sacral oedema
- raised jugular venous pressure
- hepatomegaly
- weight gain due to fluid retention
- anorexia ('cardiac cachexia')
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causes of high output HF
anaemia
arteriovenous malformation
Paget's disease
Pregnancy
thyrotoxicosis
thiamine deficiency (wet Beri-Beri)
188
FIRST line investigation for suspected HF
N-terminal pro-B-type natriuretic peptide (NT-proBNP) blood test first-line.
189
management steps after doing a NT-proBNP blod test
if levels are 'high' arrange specialist assessment (including transthoracic echocardiography) within 2 weeks
if levels are 'raised' arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks
190
is NTproBNP blood level the same as BNP blood level?
no. its a bit different:
High levels > 400 pg/ml (116 pmol/litre)
NT pro BNP > 2000 pg/ml (236 pmol/litre)
Raised levels 100-400 pg/ml (29-116 pmol/litre) 400-2000 pg/ml (47-236 pmol/litre)
Normal levels < 100 pg/ml (29 pmol/litre) < <400 pg/ml (47 pmol/litre)
191
factors other than HF that can increase BNP levels
Left ventricular hypertrophy
Ischaemia
Tachycardia
Right ventricular overload
Hypoxaemia (including pulmonary embolism)
GFR < 60 ml/min
Sepsis
COPD
Diabetes
Age > 70
Liver cirrhosis
192
factors that can decrease BNP levels
Obesity
Diuretics
ACE inhibitors
Beta-blockers
Angiotensin 2 receptor blockers
Aldosterone antagonists
193
describe classes of NYHA classification for HF
NYHA Class I
no symptoms
no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations
NYHA Class II
mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea
NYHA Class III
moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms
NYHA Class IV
severe symptoms
unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity
194
is AHF more common in existing HF (DECOMPENSATED HF) patients or as a new presentation (de-novo AHF)
MORE COMMON 66-85% in patients with background history of HF
USUALLY AFTER 65 YO
195
causes of de novo HF
ischaemia
Other less common causes of de-novo AHF are:
Viral myopathy
Toxins
196
decompensated AHF causes:
Acute coronary syndrome
Hypertensive crisis
Acute arrhythmia
Valvular disease
197
what features can helo determine therapeutic approach of AHF
Patients with heart failure are broadly characterised into 1 of 4 groups based on whether they present:
With or without hypoperfusion
With or without fluid congestion
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SYMPTOMS AND SIGNS OF AHF
Breathlessness
Reduced exercise tolerance
Oedema
Fatigue
Cyanosis
Tachycardia
Elevated jugular venous pressure
Displaced apex beat
Chest signs: classically bibasal crackles but may also cause a wheeze
S3-heart sound
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diagnostic workup for AHF
Blood tests
this is to look for any underlying abnormality such as anaemia, abnormal electrolytes or infection.
Chest X-ray
findings include pulmonary venous congestion, interstitial oedema and cardiomegaly
Echocardiogram
recommended for patients with new-onset heart failure and for patients with known heart failure who have a suspected change in cardiac function
particularly important if cardiogenic shock or suspected valvular problems
may also identify post-myocardial infarction complications
B-type natriuretic peptide
raised levels (>100mg/litre) indicate myocardial damage and are supportive of the diagnosis.
200
CHRONIC HEART FAILURE features
dyspnoea
cough: may be worse at night and associated with pink/frothy sputum
orthopnoea
paroxysmal nocturnal dyspnoea
wheeze ('cardiac wheeze')
weight loss ('cardiac cachexia'): occurs in up to 15% of patients. Remember this may be hidden by weight gained secondary to oedema
bibasal crackles on examination
signs of right-sided heart failure: raised JVP, ankle oedema and hepatomegaly
201
what is a contraindication/ side effect of GTN/ nitrates
hypotension
202
recommended treatment for all patients with ACUTE HF
IV loop diuretics
e.g. furosemide or bumetanide
203
POSSIBLE additional treatments in AHF
oxygen
this should be given in line with British Thoracic Society guidelines, i.e. keep oxygen saturations at 94-98%
vasodilators
nitrates should not be routinely given to all patients
they may, however, have a role if concomitant myocardial ischaemia, severe hypertension or regurgitant aortic or mitral valve disease
204
what to do for patients with respiratory failure during AHF
CPAP
205
DOES ANything from the chronic management of HF need to be changed during AHF
regular medication for heart failure such as beta-blockers ACE-inhibitors should be continued
beta-blockers should only be stopped if the patient has heart rate less than 50 beats per minute, second or third degree atrioventricular block, or shock
206
beta blockers licensed in the UK for heart failure
bisoprolol
carvedilol
nebivolol
207
What does research show on these management guidelines for HFpEF
beta blockers and ACEi show no improvement of mortality in HFpEF so treatment there is bit weird although still given
208
what is the standard second line treatment for HF
The standard second-line treatment is an aldosterone antagonist
these are sometimes referred to as mineralocorticoid receptor antagonists. Examples include spironolactone and eplerenone
209
what should patients on ACEi and Aldosterone antagonists be monitored for?
both cause hyperkalaemia - therefore potassium should be monitored
210
WHAT IS a medication class that is becoming recognised in the management of reduced ejection fraction HF?
SGLT-2 inhibitors
211
medication consideref 3rd line in HF with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
sacubitril-valsartan
should be initiated following ACEi or ARB wash-out period
criteria: left ventricular fraction < 35%
212
third line medication for HF if coexisting AF
digoxin
digoxin has also not been proven to reduce mortality in patients with heart failure. It may however improve symptoms due to its inotropic properties
213
THIRD LINE HF meication for afro caribbean pt
hydralazine in combination with nitrate
214
third line HF therapy in pt with a widened QRS (e.g. left bundle branch block) complex on ECG
cardiac resynchronisation therapy
215
other management considered for HF
offer annual influenza vaccine
offer one-off pneumococcal vaccine
adults usually require just one dose but those with asplenia, splenic dysfunction or chronic kidney disease need a booster every 5 years
216
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 basically calcification is also the cause here but happens earlier because there's only 2 valves so more pressure on them)
--William's syndrome (supravalvular aortic stenosis)
--post-rheumatic disease-- due to repeated inflammation and repair fibrosis
--subvalvular: HOCM
217
clinical features of symptomatic aortic stenosis
chest pain
dyspnoea
syncope / presyncope (e.g. exertional dizziness)
murmur
an ejection systolic murmur (ESM) is classically seen in -- -- aortic stenosis:
-- classically radiates to the carotids
-- nthis is decreased following the Valsalva manoeuvre
218
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
219
when is aortic valve replacement offered in aortic stenosis
if symptomatic
if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction
220
what is the treatment of choice for young, low/medium operative risk patients requiring Aortic valve replacement?
surgical AVR
Cardiovascular disease may coexist. For this reason, an angiogram is often done prior to surgery so that the procedures can be combined
221
PROCEDURES USED FOR PATIENTS requiring AVR with a high operative risk
transcatheter AVR (TAVR)
222
when is balloon valvuloplasty used as an AVR method?
may be used in children with no aortic valve calcification
in adults limited to patients with critical aortic stenosis who are not fit for valve replacement
223
what happens during aortic regurg (what phase fo cardiac cycle ect)
Aortic regurgitation (AR) is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole.
224
categories of causes of aortic regurgitation
It can be caused either by disease of the aortic valve or by distortion or dilation of the aortic root and ascending aorta.
225
causes of AR due to valve disease
chronic presentation:
rheumatic fever: the most common cause in the developing world
calcific valve disease
connective tissue diseases e.g. rheumatoid arthritis/SLE
bicuspid aortic valve (affects both the valves and the aortic root)
bicuspid aortic valve (affects both the valves and the aortic root)
acute presentation:
infective endocarditis
226
causes of AR due to aortic root disease
chronic:
bicuspid aortic valve (affects both the valves and the aortic root)
spondylarthropathies (e.g. ankylosing spondylitis)
hypertension
syphilis
Marfan's, Ehler-Danlos syndrome
acute:
aortic dissection
227
features of aortic regurgitation
-- early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
-- collapsing pulse
-- wide pulse pressure
-- Quincke's sign (nailbed pulsation)
-- De Musset's sign (head bobbing)
-- mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
228
what investigation needs to be done for suspected AR
Echocardiography
229
management of AR
medical management of any associated heart failure
surgery: aortic valve indications include
symptomatic patients with severe AR
asymptomatic patients with severe AR who have LV systolic dysfunction
230
what is the most common valve disease and second most common
aortic stenosis first
mitral regurgitation second most common (ASMR! works for this too)
231
risk factors of mitral regurgitation
Female sex
Lower body mass
Age
Renal dysfunction
Prior myocardial infarction
Prior mitral stenosis or valve prolapse
Collagen disorders e.g. Marfan's Syndrome and Ehlers-Danlos syndrome
232
causes of mitral regurgitation
post MI the papillary muscles or chordae tendinae are affected by the cardiac insult
mitral valve prolapse
infective endocarditis
rheumatic fever
congenital
233
symptoms of MR
Most patients with MR are asymptomatic]
Symptoms tend to be due to failure of the left ventricle, arrhythmias or pulmonary hypertension. This may present as fatigue, shortness of breath and oedema.
234
SIGNS OF MR
The murmur heard on auscultation of the chest is typically a pansystolic murmur described as 'blowing'.
It is heard best at the apex and radiating into the axilla.
S1 may be quiet as a result of incomplete closure of the valve. Severe MR may cause a widely split S2
235
investigations done for MR
ECG may show a broad P wave, indicative of atrial enlargement
Cardiomegaly may be seen on chest x-ray, with an enlarged left atrium and ventricle
Echocardiography is crucial to diagnosis and to assess severity
236
MEDICAL MANAGEMENT OF MR in acute cases
Medical management in acute cases involves nitrates, diuretics, positive inotropes and an intra-aortic balloon pump to increase cardiac output
237
when is surgery indicated in MR And is repair or replacement preferred in this valve disease
In acute, severe regurgitation, surgery is indicated
The evidence for repair over replacement is strong in degenerative regurgitation, and is demonstrated through lower mortality and higher survival rates
When this is not possible, valve replacement with either an artificial valve or a pig valve is considered
238
how common is mitral valve prolapse? how bad?
Mitral valve prolapse is common, occurring in around 5-10 % of the population. It is usually idiopathic but may be associated with a wide variety of cardiovascular disease and other conditions
239
what can mitral valve prolapse lead to ?
congenital heart disease: PDA, ASD
cardiomyopathy
Turner's syndrome
Marfan's syndrome, Fragile X
osteogenesis imperfecta
pseudoxanthoma elasticum
Wolff-Parkinson White syndrome
long-QT syndrome
Ehlers-Danlos Syndrome
polycystic kidney disease
240
features of mitral valve prolapse
patients may complain of atypical chest pain or palpitations
mid-systolic click (occurs later if patient squatting)
late systolic murmur (longer if patient standing)
complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death
241
causes of mitral stenosis
RHEUMATICCC FEVVVEERRRR!!!!
242
SYMPTOMS and signs of mitral stenosis
dyspnoea
↑ left atrial pressure → pulmonary venous hypertension
haemoptysis
due to pulmonary pressures and vascular congestion
may range from pink frothy sputum to sudden haemorrhage secondary to rupture of thin-walled and dilated bronchial veins
mid-late diastolic murmur (best heard in expiration)
loud S1
opening snap
indicates mitral valve leaflets are still mobile
low volume pulse
malar flush
atrial fibrillation
secondary to ↑ left atrial pressure → left atrial enlargement
243
important investigations in mitral stenosis
Chest x-ray
left atrial enlargement may be seen
Echocardiography
the normal cross-sectional area of the mitral valve is 4-6 sq cm. A 'tight' mitral stenosis implies a cross-sectional area of < 1 sq cm
244
causes of tricuspid regurgitation
Functional (secondary to RV dilation from left-sided heart failure or pulmonary hypertension)
Infective endocarditis (especially in IV drug users)
Carcinoid syndrome
Rheumatic heart disease (rare)
245
signs of tricuspid regurgitation
Holosystolic murmur at left lower sternal border, louder on inspiration (Carvallo’s sign)
Raised JVP with prominent v-waves
Hepatomegaly, ascites, peripheral oedema
246
pulmonary regurg some stuff (case and symptoms)
ulmonary hypertension, post-surgical (e.g. after repair of Tetralogy of Fallot)
Often asymptomatic, may hear a diastolic murmur (Graham Steell murmur)
247
pulmonary stenosis some stuff
Usually congenital
Ejection systolic murmur at upper left sternal edge, with an ejection click
May cause RV hypertrophy → right heart failure
