Cardiology Flashcards
(266 cards)
1
Q
on an ecg one large square is how much in time
A
0.2seconds or 200ms
2
Q
on an ecg one small square is how long in time
A
0.04 seconds or 40ms
3
Q
how many large squares per second in an ecg
A
5 large squares per second
4
Q
what is the PR interval and how long should it be
A
time from the onset of the P wave to the start of the QRS complex
it should normally be 120-200ms
this is 3-5 small squares
5
Q
draw the ecg axis diagram
A
6
Q
normal axis is from what degrees to what degrees
A
-30 degrees to +90 degrees
7
Q
left axis deviation will look like what
A
QRS predominantly negative in VF II and III
QRS predominantly positive in VL and I
8
Q
right axis deviation will look like what
A
QRS predominantly negative in I
QRS predominantly positive in III
9
Q
which leads look at the septum
A
V3 and V4
10
Q
what is the transition point
A
- the v1 lead looks at the heart from the right
- it begins with a small septal r wave as the septum is depolarised left to right initially
- then as the left ventricle depolarises there follows a large downwards S
- the v1 complex is therefore predominantly negative
- the v6 lead looks at the heart from the left
- it begins with a small downwards Q as the septum is initially depolarised left to right
- then there is a large upwards R wave as the left ventricle is depolarised
- the v6 complex is therefore predominantly positive
- the transition point is the point at which the R waves and the S waves are of equal size
- it is usually around v3-v4
11
Q
what is the significance of the transition point
A
- it can shift with changing shape of the heart
- with right ventricular hypertrophy the transition point would shift to the left
- this would mean that it would be around v5-v6 rather than v3-v4
- it is as if, seen from the perspective of the feet, the heart has rotated clockwise
12
Q
what is first degree heart block
A
it is when the pr interval is longer than 200ms
it’s ‘marked first degree heart block’ if >300ms
13
Q
what is second degree heart block
A
- mobitz i (wenckeback)
- progressive lengthening of pr
- followed by a dropped QRS complex
- pr then goes back to being shorter and the cycle continues
- mobitz ii
- PR interval is constant but there is an occasional dropped QRS
- there may be two or three or four P waves for every successful QRS in which case it is given a ratio 2:2 or 3:1 etc
- PR interval is constant but there is an occasional dropped QRS
14
Q
what is third degree heart block
A
atrial contraction may be normal but no beats are conducted to the ventricles themselves
ventricular contraction is maintained by ventricular escape rhythms
15
Q
what does blockage of both bundle branches look like
A
it has the same effect as a complete block of the his bundle and resembles complete heart block
16
Q
why does right bundle branch block look like that
A
- best seen in v1 where there is an RSR pattern
- upwards deflection as septum initially depolarised from left to right
- then s wave as the left ventricle is depolarised as normal
- it takes longer for the right ventricle to be depolarised so there then follows a second R wave as the right ventricle is depolarised after the left
- in v6 there is a wide deep qrs
- initially a q as the septum is depolarised left to right
- then an R wave as the left ventricle is depolarised
- then follows a deep wide s wave as the right ventricle catches up
- right bundle branch block is only significant if the qrs is longer than 120ms
17
Q
why does left bundle branch block look like that
A
- if conduction down the left bundle branch fails then the septum is depolarised from right to left
- in V1 this appears as a small q wave
- then the right ventricle is depolarised before the left so there is then an r wave in v1
- subsequent depolarisation of the left ventricle then causes an s wave in v1
- in V6 the initial right to left depolarisation of the septum causes a small r wave
- then follows a small (like a notch) s wave as the right ventricle is depolarised
- then v6 shows another R wave as the left ventricle catches up
- in V1 this appears as a small q wave
18
Q
in summary how does right bundle branch block appear
A
best seen in v1
there is an RSR pattern
19
Q
in summary how does LBBB appear
A
best seen in v6 where there is a broad qrs with a notched top
the complete picture with a w shape in v1 is often not fully visible
20
Q
what happens in atrial tachycardia
A
depolarisation is from an origin in the atria that is different to the sa node
the av node cannot conduct rates fasterr than 200/min so there may be a physiological block
21
Q
what happens in atrial flutter
A
if there atrial rate is >250/minute then there is no baseline between p waves
22
Q
what happens in junctional/nodal tachycardia
A
the depolarisation originates from the area around the av node
therefore the atria and the ventricles are depolarised at the same time
therefore p wave will be very close to the QRS complex or may be lost within it
23
Q
what happens in wolff parkinson white syndrome
A
- some people have an accessory bundle connecting the atria and the ventricles
- there is no AV node delaying contraction
- this provides pre-excitation to the ventricles
- therefore there is a short PR interval and the QRS has a wide slurred upstroke called a delta wave
- the second part of the QRS is normal as the excitation from the his bundle catches up
- the his bundle and the accessory bundle can together form a re-entry circuit that causes tachycardias
24
Q
what are the 6 questions to ask yourself when identifying abnormal ecg rhythms
A
- is the abnormality occasional or sustained
- are there p waves
- what is the P:QRS ratio
- are the ventricles contracting regularly or irregularly
- is the QRS a normal shape
- what is the ventricular rate
25
identify the rhythms
26
what are the two important abnormalities in form of the p wave
* peaked p wave
* right atrial hypertrophy
* pulmonary hypertension
* tricuspid valve stenosis
* broad and bifid p wave
* left atrial hypertrophy
* usually due to mitral stenosis
27
what are the 4 characteristics of a normal QRS
1. duration no longer than 120ms (3 little squares)
2. in a right ventricular lead the (V1) the S is greater than the R
3. in a left ventricular lead (V6) the R is less than 25mm
4. left ventricular leads show a Q wave due to septal depolarisation which is initially left to right but these are less than 1mm across and 2mm deep
28
what are the ECG findings of PE
* in many cases there is a normal ecg
* sinus tachycardia is the most common finding
* but there may be findings of acute cor pulmonale
* S1Q3T3
* large S wave in lead 1
* pathological Q wave in lead 3
* inverted T wave in lead 3
29
what are the ecg findings of right ventricular hypertrophy
* peaked p waves (as it normally accompanies right atrial hypertrophy)
* right axis deviation
* tall r waves in v1
* maybe right bundle branch block
* inverted T waves which are normal in v1 spread across to v2 and v3
* transition point shifts to the left with a deep s wave persisting in v6
30
in which leads are q waves normal
in the left ventricular leads
31
when are q waves abnormal
when they are greater than 1 small square in width (40ms) and 2mm in depth
32
what does a q wave of more than 1 small square in width (40ms) and 2mm in depth signify
MI
can be old or new as once q waves appear they rarely go
33
why are q waves from MI
* because ventricles depolarise from inside to outside
* therefore an area that's not depolarising will record as a cavity potential
* therefore a lead looking at that area will record a q wave
* this will therefore be the case for anterior, lateral and anterolateral MIs
* not posterior MIs as there's no leads looking at the back typically
34
how does a posterior MI look on ECG
* there may or may not be ST elevation
* left ventricular depolarisation no longer overshadows right ventricular in V1
* therefore V1 shows a tall R wave
* this is similar to as in right ventricular hypertrophy but doesn't have the other features of rvh
35
st elevation is due to
MI or pericarditis
pericarditis it will be in all of the leads whereas in MI it's usually localised
36
horizontal depression of the ST segment means
ischaemia rather than infarction
37
downward sloping ST segments are due to treatment with digoxin
38
T waves are normally inverted in which leads
* VR
* V1
* sometimes in III
* sometimes in V2
* in V3 in some black people
39
what is the effect of digoxin in the ecg
af
downward sloping st
inverted t waves
40
what's the process of stemi ecg changes
* the first abnormality seen in st elevation
* then Q waves appear and the T wave becomes inverted
* the st segment then returns to baseline
41
nstemi ecg changes
not full thickness so no Q wave and no ST elevation
but there will still be t wave inversion
42
main ecg finding of left ventricular hypertrophy
* there may be left axis deviation
* but the main thing is that there will be inverted t waves in the lateral leads
* I, II, aVL, v5 and v6
43
why can t wave inversion be seen in bundle branch block
because abnormal depolarisation can lead to abnormal repolarisation
44
what are the 4 situations you can see t wave inversion in?
ischaemia
ventricular hypertrophy
bundle branch block
digoxin treatment
45
what does low sodium do to the ecg
it doesn't change the ecg at all
46
low k+ causes what ecg changes
T wave flattening
hump on the end of the T wave called the U wave
47
high potassium does what to the ecg
peaked t waves with disappearance of the ST segment
QRS may be widened
48
low calcium does what to the ecg
long qt
49
high calcium does what to the ecg
short qt
50
what investigations for angina
ECG
FBC
lipid profile
HbA1c
LFTs (before statins)
U&E (before ACEIs)
TFTs
CT Coronary angiography
51
management of angina
* 1st line:
* lifestyle advice
* secondary prevention:
* antiplatelet
* aspirin OR clopidogrel
* OR aspirin AND clopidogrel
* statin
* atorvastatin 10mg PO OD
* if symptomatic:
* sublingual GTN spray +/-
* beta blocker (metoprolol) +/-
* calcium channel blocker (nifedipine) +/-
* long acting nitrate (isosorbide mononitrate PO)
52
explain PCI
***Percutaneous Coronary Intervention (PCI)*** with ***coronary angioplasty*** (dilating the blood vessel with a balloon and/or inserting a stent) is offered to patients with “proximal or extensive disease” on CT coronary angiography. This involves putting a catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance and injecting contrast so that the coronary arteries and any areas of stenosis are highlighted on the xray images. This can then be treated with balloon dilatation followed by insertion of a stent.
53
explain cabg
***Coronary Artery Bypass Graft (CABG)*** surgery may be offered to patients with severe stenosis. This involves opening the chest along the sternum (causing a ***midline sternotomy scar***), taking a graft vein from the patient’s leg (usually the ***great saphenous vein***) and sewing it on to the affected coronary artery to bypass the stenosis. The recovery is slower and the complication rate is higher than PCI.
54
the right coronary artery supplies the
* Right atrium
* Right ventricle
* Inferior aspect of left ventricle
* Posterior septal area
55
the circumflex artery supplies the
* Left atrium
* Posterior aspect of left ventricle
56
the left anterior descending artery supplies the
* Anterior aspect of left ventricle
* Anterior aspect of septum
57
different sub-devisions of acs
* if there's st elevation or new LBBB it's a stemi
* it's nstemi if no st elivation but trops are high OR there's other ecg changes such as
* st depression
* t wave inversion
* pathological q waves
* if trops normal and there's no pathological changes on ecg then it's unstable angina or another cause such as MSK
58
anterolateral infarct is likely which artery and would show in which leads
left coronary artery
aVL, V3-6, I
59
anterior infarct is likely which artery and would show in which leads
LAD
V1-4
60
lateral infarct is likely which artery and would show in which leads
I, aVL, V5-6
61
inferior infarct is likely which artery and would show in which leads?
right coronary artery
II, III and aVF
62
alternative causes of raised troponins
* Chronic renal failure
* Sepsis
* Myocarditis
* Aortic dissection
* Pulmonary embolism
63
what are serial troponins
baseline and 6 or 12 hours after onset of symptoms
64
explain thrombolysis
***Thrombolysis*** involves injecting a ***fibrinolytic*** medication (they break down ***fibrin***) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous. Some examples of thrombolytic agents are ***streptokinase***, ***alteplase*** and ***tenecteplase***.
65
ideal treatment for STEMI
Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for either:
* ***Primary PCI*** (if available within 2 hours of presentation)
* ***Thrombolysis*** (if PCI not available within 2 hours)
The local cardiac centre will advise about further management (such as further loading with aspirin and ticagrelor).
66
acute nstemi treatment
* BATMAN
**B** – **Beta-blockers** unless contraindicated
**A** – **A**spirin 300mg stat dose
**T** – **T**icagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)
**M** – **M**orphine titrated to control pain
**A** – **A**nticoagulant: Fondaparinux (unless high bleeding risk)
**N** – **N**itrates (e.g. GTN) to relieve coronary artery spasm
Give oxygen only if their oxygen saturations are dropping (i.e. \<95%).
67
scoring system for NSTEMI mortality and what it means for treatment
**GRACE Score**
* \<5% Low Risk
* 5-10% Medium Risk
* \>10% High Risk
If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.
68
what's included in the grace score
Age
Heart rate/pulse
Systolic BP
Creatinine
Cardiac arrest at admission
CHF
Pulmonary edema
Cardiogenic shock
69
what is dressler's syndrome?
* occurs about 2-3 weeks after an MI
* it's an autoimmune pericarditis
70
how does dressler's syndrome present?
***pleuritic*** chest pain, low grade fever and a ***pericardial rub*** on auscultation. It can cause a ***pericardial effusion*** and rarely a ***pericardial tamponade***
71
how do you diagnose dressler's syndrome?
diagnosis can be made with an **ECG** (***global ST elevation*** and ***T wave inversion***), **echocardiogram** (***pericardial effusion***) and raised **inflammatory markers** (***CRP*** and ***ESR***).
72
management of dressler's syndrome
**NSAIDs** (***aspirin*** / ***ibuprofen***) and in more severe cases **steroids** (***prednisolone***). They may need ***pericardiocentesis*** to remove fluid from around the heart.
73
triggers for acute left ventricular failure
* Iatrogenic (e.g. too much fluids in an elderly patient with poor LV function)
* Sepsis
* MI
* Arrhythmias
74
what is the function of BNP
To relax the smooth muscle in blood vessels. This reduces the ***systemic vascular resistance*** making it easier for the heart to pump blood through the system.
BNP also acts on the kidneys as a diuretic to promote the excretion of more water in the urine. This reduces the circulating volume helping to improve the function of the heart.
75
non heart failure causes of a raised BNP
* Tachycardia
* Sepsis
* Pulmonary embolism
* Renal impairment
* COPD
it is very sensitive not specific
76
work up for acute LVF
* ECG (to look for ischaemia and arrhythmias)
* Arterial Blood Gas (ABG)
* Chest Xray
* Bloods (routine bloods for infection, kidney function, ***BNP*** and consider ***troponin*** if suspecting MI)
77
presentation of acute left ventricular failure
* Shortness of breath
* Cough (frothy white/pink sputum)
* Reduced oxygen saturations
* 3rd Heart Sound
* Bilateral basal crackles (sounding “wet”) on auscultation
* Hypotension in severe cases (***cardiogenic shock***)
There may also be signs and symptoms related to **underlying cause**, for example:
* Chest pain in ACS
* Fever in sepsis
* Palpitations in arrhythmias
78
what is a normal ejection fraction
anything above 50%
79
normal pulmonary artery pressure at rest
**18 to 25 mmHg**
80
heart failure chest x ray findings
* dilated upper airway vessels (upper lobe diversion)
* cardiomegaly (cardiothoracic ratio of \>0.5)
* kerly B lines
* bilateral pleural effusions
81
management of acute left ventricular failure
* Pour SOD
* Pour away (stop) IV fluids
* Sit the patient upright
* Oxygen
* Diuretics (e.g. 40mg IV furosemide)
82
why does PND happen at night
* fluid over larger area as laid down
* respiratory centre is less responsive during sleep: resp effort doesn't increase in response to hypoxia
* less adrenaline during sleep so myocardium is more relaxed and cardiac output is worse
83
what are the different types of heart failure
* heart failure with reduced ejection fraction
* LVEF \<40%
* heart failure with mid range ejection fraction
* LVEF 40%-49%
* raised BNP
* and at least one other criterion
* relevant structural heart disease (e.g., left ventricular hypertrophy [LVH] or left atrial enlargement),
* diastolic dysfunction
* heart failure with preserved ejection fraction
* LVEF \>50%
* raised BNP
* and at least one other criterion
* relevant structural heart disease
* diastolic dysfunction
84
NHYA heart failure classification
Class I: Mild. No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitations, or dyspnoea.
Class II: Mild. Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitations, or dyspnoea.
Class III: Moderate. Marked limitation of physical activity. Comfortable at rest, but gentle activity causes fatigue, palpitations, or dyspnoea.
Class IV: Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.
85
when to refer chronic heart failure
* refer those with NT-proBNP above 2000 to a specialist for an echo within two weeks
* if between 400-2000 then they need an echo within 6 weeks
86
management of acute heart failure with reduced ejection fraction
* Furosemide titrated according to symptoms
* prescribe both an ace inhibitor and a B blocker but one at a time
* if fluid overload an ace inhibitor first
* if cant tolerate then an ARB
* if angina then a B blocker first
* aldosterone antagonist if not controlled with above
* spironolactone or eplerenone
* also
* yearly flu and pneumococcal vaccine
* exercise rehab group for heart failure
* treat cause if known e.g. surgical treatment of valve problems
87
what is cor pulmonale
right sided heart failure caused by respiratory disease
88
what are the cause of cor pulmonale
* COPD is the **most common** cause
* Pulmonary Embolism
* Interstitial Lung Disease
* Cystic Fibrosis
* Primary Pulmonary Hypertension
89
why might you get pulsatile hepatomegaly
in right sided heart failure with tricuspid regurgitation
90
above what threshold do you diagnose hypertension
blood pressure above 140/90 in clinic or 135/85 with ambulatory or home readings.
91
what is the difference between primary (essential) and secondary hypertension? what is more common?
primary (essential hypertension) is 95% of all hypertension and means there is not a known cause
secondary hypertension has a known cause
92
causes of secondary hypertension
* Consider in patients aged under 40
* Remember with the mnemonic ROPE
* **R** – **R**enal disease. This is the most common cause of secondary hypertension. If the blood pressure is very high or does not respond to treatment consider ***renal artery stenosis***.
* **O** – **O**besity
* **P** – ***Pregnancy induced hypertension*** / ***pre-eclampsia***
* **E** – **E**ndocrine. Most endocrine conditions can cause hypertension
93
main endocrine consideration for secondary **hypertension**
***hyperaldosteronism*** (“***Conns syndrome***”) as this may represent 2.5% of new hypertension. A simple test for this is a ***renin***:***aldosterone ratio*** blood test.
94
patients with type two diabetes should have hypertension screenings how frequently?
every year
95
how frequently should the general population be screened for high blood pressure?
every five years
96
what investigations should all patients with new diagnoses of hypertension get
* ***Urine*** ***albumin:creatinine ratio*** for proteinuria and ***dipstick*** for microscopic haematuria to assess for kidney damage
* ***Bloods*** for HbA1c, renal function and lipids
* ***Fundus examination*** for hypertensive retinopathy
* ***ECG*** for cardiac abnormalities
97
what are the different stages of hypertension
98
do the flow diagram for hypertension treatment
99
blood pressure targets in people under 80
Clinic BP: \<140/90 mmHg
ABPM/HBPM: \<135/85 mmHg
100
blood pressure targets in people over 80
Clinic BP: \<150/90 mmHg
ABPM/HBPM: \<145/85 mmHg
101
what is the third heart sound
it's the chordae tendonae twanging open like guitar string
can be normal in people aged 15-40
can indicate heart failure in people over 40
102
what are the 4 valve areas on the chest
* ***Pulmonary***: 2nd I.C.S left sternal border
* ***Aortic***: 2nd I.C.S right sternal border
* ***Tricuspid***: 5th I.C.S left sternal border
* ***Mitral***: 5th I.C.S mid clavicular line (apex area)
103
what are the special manoeuvres for listening to certain murmurs
* Patient on their left hand side (***mitral stenosis***)
* Patient sat up, learning forward and holding exhalation (***aortic regurgitation***)
104
mitral stenosis is caused by
* Rheumatic Heart Disease
* Infective Endocarditis
105
what kind of murmur is mitral stenosis
***mid-diastolic***, **low pitched** “rumbling” murmur due to a low velocity of blood flow. There will be a loud S1 due to thick valves requiring a large systolic force to shut, then shutting suddenly
106
describe the sound of mitral regurgitation
***pan-systolic***, **high pitched** “whistling” murmur due to high velocity blood flow through the leaky valve. The murmur radiates to left axilla. You may hear a third heart sound.
107
causes of mitral regurgitation
* Idiopathic weakening of the valve with age
* Ischaemic heart disease
* Infective Endocarditis
* Rheumatic Heart Disease
* Connective tissue disorders such as ***Ehlers Danlos syndrome*** or ***Marfan syndrome***
108
describe the murmur in aortic stenosis
***ejection-systolic***, **high pitched** murmur (high velocity of systole). This has a ***crescendo-decrescendo*** character due to the speed of blood flow across the value during the different periods of ***systole***
***radiates into the carotids***
109
causes of aortic stenosis
* Idiopathic age related calcification
* Rheumatic Heart Disease
110
what is an austin flint murmur
heard at the ***apex*** and is an early diastolic “**rumbling**” murmur. This is caused by blood flowing back through the aortic valve and over the mitral valve causing it to vibrate.
111
what are the causes of aortic regurgitation
* Idiopathic age related weakness
* Connective tissue disorders such as ***Ehlers Danlos syndrome*** or ***Marfan syndrome***
112
where do bioprosthetic heart valves come from and how long do they last
they come from pigs and they last around 10 years
113
how long do mechanical heart valves last
well over 20 years
114
what is the target INR if someone has a mechanical heart valve
2.5-3.5
115
major complications of mechanical heart valves
* ***Thrombus*** formation (blood stagnates and clots)
* ***Infective endocarditis*** (infection in prosthesis)
* ***Haemolysis*** causing anaemia (blood gets churned up in the valve)
116
A click replaces S1 for metallic valve replacing which valve
mitral
117
A click replaces S1 for metallic valve replacing which valve
aortic
118
what is tavi the treatment for
***severe aortic stenosis***
119
explain tavi
It involves local or general anaesthetic, inserting a catheter in to the ***femoral artery***, feeding a wire under ***xray guidance*** to the location of their aortic valve, then inflating a balloon to stretch the stenosed aortic valve and implanting a ***bioprosthetic valve*** in the location of the aortic valve.
valve is bioprosthetic so they don't require warfarin
120
what are the rates of infective endocarditis in valve replacement patients
what are the usual causative organisms
* 2.5% of patients having a surgical valve replacement.
* 1.5% of patients having TAVI
* This is usually caused by one of three ***gram positive cocci*** organisms:
* Staphylococcus
* Streptococcus
* Enterococcus
121
there are two differentials for an irregularly irregular pulse - what are they?
* ***Atrial fibrillation***
* ***Ventricular ectopics***
122
what is valvular AF
***Valvular AF*** is defined as patients with AF who also have moderate or severe ***mitral stenosis*** or a ***mechanical heart valve***. The assumption is that the valvular pathology itself has lead to the atrial fibrillation. AF without valve pathology or with other valve pathology such as mitral regurgitation or aortic stenosis is classed as ***non-valvular AF.***
123
what are the most common causes of AF
* remember that AF affects mrs SMITH
* Sepsis
* Mitral valve stenosis
* Ischaemic heart disease
* Thyrotoxicosis
* Hypertension
124
draw flow diagram of how to treat AF in the acute setting
125
what is the first line treatment for AF
rate control with either a beta blocker or a rate limiting calcium channel blocker such as verapamil or diltiazem
126
what do you need to do for all patients with AF
[_CHA2DS2VAS_](https://cks.nice.org.uk/topics/atrial-fibrillation/management/management-of-af/#the-cha2ds2vasc-score-tool)c and ORBIT to assess risk of clot/bleeding
127
what is [CHA2DS2VASc and how should it be used](https://cks.nice.org.uk/topics/atrial-fibrillation/management/management-of-af/#the-cha2ds2vasc-score-tool)
* **C**ongestive heart failure = 1
* **H**ypertension = 1
* **A**ge older than or equal to 75 years = 2
* **D**iabetes mellitus = 1
* **S**troke/TIA = 2
* **V**ascular disease (prior myocardial infarction, peripheral arterial disease, or aortic plaque) = 1
* **A**ge 65–74 years = 1
* **S**ex category (female) = 1
offer anticoagulation with a DOAC if \>2 in women or \>1 in men
128
what anticoagulation should you use in AF
a doac such as rivaroxiban or warfarin if doacs are contraindicated
129
what tool should you use to assess risk of bleeding in a patient with atrial fibrillation
ORBIT (it used to be hasbled)
130
what is the orbit risk assessment tool
131
in delayed cardioversion how long should they be anticoagulated for and why
In **delayed cardioversion** the patient should be ***anticoagulated*** (see below) for a minimum of 3 weeks prior to ***cardioversion***. Anticoagulation is essential because during the 48 hours prior to cardioversion they may have developed a blood clot in the atria and reverting them back to sinus rhythm carries a high risk of mobilising that clot and causing a ***stroke***.
They should have **rate control** whilst waiting for cardioversion.
132
how do you treat paroxysmal atrial fibrillation
patients still need to be anticoagulated according to ***CHADSVASc***
they can also use a pill in the pocket approach for when symptoms come on
the pill of choice is normally flecanide
133
when should you avoid flecanide?
Avoid ***flecanide*** in ***atrial flutter*** as it can cause 1:1 AV conduction and resulting in a significant tachycardia.
134
what is the half life of warfarin
1-3 days
135
what is the half life of doacs
7-15 hours
136
what can be used to reverse apixaban and rivaroxaban in the case of life threatening bleeding?
***Andexanet alfa***
137
what can be used to reverse dabigatran in the case of life threatening bleeding
***Idarucizumab***
138
which drug should not be used in VT
verapamil as it may precipitate cardiac arrest
139
broad complex tachycardias are from where in origin
* they could be supraventricular with aberrant conduction
* they could also be ventricular in origin
* in a peri-arrest situation you should assume them to be ventricular in origin
140
what is the definition of ventricular tachycardia
* broad complex tachycardia originating from a ventricular focus
* 3 or more ventricular extrasystoles in succession at a rate of more than 120 bpm
141
how to treat tachycardia with pulse - draw algorithm
142
what's included in hasbled
143
what's included in hasbled
144
what are the four cardiac arrest rhythms and which are shockable
**Shockable rhythms:**
* ***Ventricular tachycardia***
* ***Ventricular fibrillation***
**Non-shockable rhythms:**
* ***Pulseless electrical activity*** (all electrical activity except VF/VT, including sinus rhythm without a pulse)
* ***Asystole*** (no significant electrical activity)
145
Narrow complex tachycardia in a stable patient can be:
how would you treat each?
* ***Atrial fibrillation*** – rate control with a beta blocker or diltiazem (calcium channel blocker)
* ***Atrial flutter*** – control rate with a beta blocker
* ***Supraventricular tachycardias*** – treat with vagal manoeuvres and adenosine
146
broad complex tachycardia in a stable patient could be what? and how would you treat each?
* ***Ventricular tachycardia*** or unclear – amiodarone infusion
* If known ***SVT with bundle branch block*** treat as normal SVT
* If irregular may be AF variation – seek expert help
147
what are the rates involved in atrial flutter and why
* atrial flutter is due to a re-entry loop
* this stimulates atria at 300bpm
* every second atrial stimulation is conducted to the ventricles
* this gives a ventricular rate of 150bpm
148
what is the treatment for atrial flutter
* **Rate/rhythm control** with beta blockers or cardioversion
* Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
* ***Radiofrequency ablation*** of the re-entrant rhythm
* ***Anticoagulation*** based on CHA2DS2VASc score
149
what are the three types of SVT
* “***Atrioventricular nodal re-entrant tachycardia***” is when the re-entry point is back through the AV node.
* “***Atrioventricular re-entrant tachycardia***” is when the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome).
* “***Atrial tachycardia***” is where the electrical signal originates in the atria somewhere other than the ***sinoatrial node***.
150
how does adenosine work
* Adenosine interrupts the ***AV node*** / ***accessory pathway*** during SVT and “resets” it back to sinus rhythm.
* It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway.
* It will often cause a brief period of ***asystole*** or ***bradycardia*** that can be scary for the patient and doctor, however it is quickly metabolised and sinus rhythm should return.
151
in which patients should adenosine be avoided
* patients with
* asthma
* COPD
* heart failure
* heart block
* severe hypotension
152
how should you administer adenosine
* Give as a fast IV bolus into a large proximal cannula (e.g. grey cannula in the ***antecubital fossa***)
* Initially **6mg**, then **12mg** and further **12mg** if no improvement between doses
* warn about feeling of impending doom
153
what is the definitive treatment for wolff parkinson white syndrome
radiofrequency ablation of the bundle of kent
154
how does radiofrequency ablation work
* ***Catheter ablation*** is performed in a electrophysiology laboratory, often called a “***cath lab***”.
* General anaesthetic
* Inserting a catheter in to the ***femoral veins*** and feeding a wire through the ***venous system*** under ***xray guidance*** to the heart.
* Once in the heart it is placed against different areas to test the electrical signals at that point. This way the operator can hopefully find the location of any abnormal electrical pathways.
* The operator may try to induce the arrhythmia to make the abnormal pathways easier to find.
* Once identified, ***radiofrequency ablation*** (**heat**) is applied to burn the abnormal area of electrical activity.
* This leaves scar tissue that does not conduct the electrical activity.
155
radiofrequency ablation is curative for which types of arrhythmia
* ***Atrial Fibrillation***
* ***Atrial Flutter***
* ***Supraventricular Tachycardias***
* ***Wolff-Parkinson-White Syndrome***
156
causes of a long QT
* ***Long QT Syndrome*** (inherited)
* Medications (***antipsychotics***, ***citalopram***, ***flecainide***, ***sotalol***, ***amiodarone***, ***macrolide antibiotics***)
* Electrolyte Disturbance (***hypokalaemia***, ***hypomagnesaemia***, ***hypocalcaemia***)
157
acute management of torsades de pointes
* Correct the cause (electrolyte disturbances or medications)
* Magnesium infusion (even if they have a normal serum magnesium)
* Defibrillation if VT occurs
158
what is bigeminy
* it is when a ventricular ectopic happens after every sinus beat
* so normal sinus beat
* followed by broad QRS without a P wave
159
draw the bradycardia algorithm
160
first line management of acute pericarditis is
NSAID and colchicine
161
features of pericarditis
* chest pain: may be pleuritic. Is often relieved by sitting forwards
* other symptoms include non-productive cough, dyspnoea and flu-like symptoms
* pericardial rub
* tachypnoea
* tachycardia
162
ecg changes in pericarditis
* the changes in pericarditis are often global/widespread, as opposed to the 'territories' seen in ischaemic events
* 'saddle-shaped' ST elevation
* PR depression: most specific ECG marker for pericarditis
163
causes of pericarditis
* most common: coxsacie virus
* TB
* uraemia (causes fibrinous pericarditis)
* trauma
* post MI (dressler's syndrome)
164
side effects of adenosine
* flushing
* nausea
* sweating
* bronchospasm
* chest pain
* feeling of impending doom
165
adenosine half life
8-10 seconds
166
what is the investigation of choice if you suspect PE in a patient with renal failure
V/Q scan since it uses radio nucleotides rather than contrast (as used in CTPA which would otherwise be gold standard) so there is no risk of further renal impairment
167
what is the investigation of choice if you suspect PE in a pregnant patient
V/Q scan since radiation dose from the injected radio-nucleotides is lower than the dose absorbed from CT imaging (so no CTPA)
168
How do you rule out PE
* all perc criteria must be absent
* you should only use perc when you have a low clinical suspicion of PE
* HADCLOTS
* Hormones
* age \>50
* DVT/PE history
* Coughing blood
* Leg swelling
* O2 \<94
* Tachycardia \>100
* Surgery/trauma in last 4 wks
169
if you suspect PE what score should you do and how do you interpret the results?
170
based on someone's level 2 wells score how should you act
* PE Likely (\>4 points)
* immediate CTPA
* if CTPA delay then interim therapeutic anticoagulation
* this means a DOAC since these can be continued if the result is positive
* if PE unlikely (4 points or less)
* D-Dimer with result within 4 hours (or ITAC if delay)
* if D-dimer positive then immediate CTPA
* if delay in CTPA then give interim therapeutic anticoagulation until scan is performed
* if D-dimer negative then PE unlikely consider another diagnosis
171
ECG changes in PE
* the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - 'S1Q3T3'.
* However, this change is seen in no more than 20% of patients
* right bundle branch block and right axis deviation are also associated with PE
* sinus tachycardia may also be seen
172
Chest x ray findings in PE
* a chest x-ray is recommended for all patients to exclude other pathology
* however, it is typically normal in PE
* possible findings include a wedge-shaped opacification
173
Chest x ray findings in PE
* a chest x-ray is recommended for all patients to exclude other pathology
* however, it is typically normal in PE
* possible findings include a wedge-shaped opacification
174
What are the first line antihypertensives in diabetics regardless of age
* ACE inhibitors or angiotensin II receptor agonists since they have a renoprotective effect in diabetes
175
features of hypercalcaemia
* 'bones, stones, groans and psychic moans'
* corneal calcification
* shortened QT interval on ECG
* hypertension
176
What is the most common cause of high calcium
cancer
177
what is ABCD2 and what is it used to test
Prognostic score for risk stratifying patients who've had a suspected TIA
178
how is heart failure classed
nyha classification
179
what is DAS28
Measure of disease activity in rheumatoid arthritis
1. count the number of swollen joints (out of the 28),
2. count the number of tender joints (out of the 28),
3. take blood to measure the erythrocyte sedimentation rate (ESR) or C reactive protein (CRP),
4. ask you (the patient) to make a ‘global assessment of health’ (indicated by marking a 10 cm line between very good and very bad).
These results are then fed into a complex mathematical formula to produce the overall disease activity score. A DAS28 of greater than 5.1 implies active disease, less than 3.2 low disease activity, and less than 2.6 remission.
180
what is wells score
Helps estimate the risk of a patient having a deep vein thrombosis
181
what are the H's and the Ts of reversible cardiac arrest
182
in ALS you need to give chest compressions and assess for a shockable rhythm every 2 minutes (and administer a shock if it's shockable) what other treatment should you do
* Give oxygen
* Intravenous or intraosseous access
* Give adrenaline every 3–5 min
* Give amiodarone after 3 shocks
* Identify and treat reversible causes
183
when do you give adrenaline in ALS and how much by which route
* adrenaline 1 mg as soon as possible for non-shockable rhythms
* during a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have restarted after the third shock
* repeat adrenaline 1mg every 3-5 minutes whilst ALS continues
* IV is first line but if not then IO
184
when is amiodarone given in ALS and how much
* 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
185
investigations for palpitations
* first line
* ECG
* only captures for a few seconds so may miss episodic arrhythmias but may catch linked abnormalities
* TFTs
* U&E
* FBC
* if nothing found
* Holter monitoring
* if nothing found
* external loop recorder
* implantable loop recorder
186
what is the inheritance pattern of hypertrophic obstructive cardiomyopathy
autosomal dominant
187
what is the most common cause of sudden cardiac death in the young
hypertrophic obstructive cardiomyopathy HOCM
188
what is the pathophysiology of hypertrophic obstructive cardiomyopathy
* mutation in gene encoding beta myosin
* results in diastolic dysfunction
* left ventricle hypertrophy leads to decreased compliance leads to decreased cardiac output
* characterised by myofibrillar hypertrophy with chaotic and disorganised fashion myocytes and fibrosis on biopsy
189
features of hypertrophic obstructive cardiomyopathy
* can be asymptomatic
* angina syncope
* typically following exercise
* due to subaortic hypertrophy of ventricular septum resulting in functional aortic stenosis
* sudden death
* arrhythmias
* heart failure
* ejection systolic murmur
* jerky pulse with a double apex beat
190
what are the echo findings of hypertrophic obstructive cardiomyopathy
* mnemonic: MR SAM ASH
* mitral regurge (MR)
* systolic anterior motion (SAM) of the anterior mitral valve leaflet
* asymetric hypertrophy (ASH)
191
what are the stages of hypertension
192
how do you decide whether to treat hypertension
193
how do you manage hypertension
194
what are ecg changes and the coronary artery implicated for the following infarctions:
anteroseptal
inferior
anterolateral
lateral
posterior
195
what is the first line treatment for heart failure
The first-line treatment for all patients is both an **ACE-inhibitor** and a **beta-blocker**
* generally, one drug should be started at a time. NICE advise that clinical judgement is used when determining which one to start first
* beta-blockers licensed to treat heart failure in the UK include bisoprolol, carvedilol, and nebivolol.
* ACE-inhibitors and beta-blockers have no effect on mortality in heart failure with *preserved* ejection fraction
196
what is second line treatment for heart failure
Second-line treatment is an **aldosterone antagonist**
* Examples include spironolactone and eplerenone
* it should be remembered that both ACE inhibitors (which the patient is likely to already be on) and aldosterone antagonists both cause hyperkalaemia - therefore potassium should be monitored
197
what are the third line treatments for heart failure
* Third-line treatment should be initiated by a specialist.
* digoxin if coexistant AF
* hydralazine if afrocarribean
* cardiac resynchronization therapy if broad QRS
198
what are the different criteria for the different third line treatments in heart failure
* ivabradine
* criteria: sinus rhythm \> 75/min and a left ventricular fraction \< 35%
* sacubitril-valsartan
* criteria: left ventricular fraction \< 35%
* is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
* should be initiated following ACEi or ARB wash-out period
* 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
* it is strongly indicated if there is coexistent atrial fibrillation
* hydralazine in combination with nitrate
* this may be particularly indicated in Afro-Caribbean patients
* cardiac resynchronisation therapy
* indications include a widened QRS (e.g. left bundle branch block) complex on ECG
199
what are the vaccine requirements for people with heart failure
* 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
200
when might you hear splitting of the first heart sound?
when the mitral valve closes significantly before the tricuspid valve, producing two separate audible sounds. Inspiration is a common cause of this as it delays the closure of the tricuspid valve
201
when might you hear a soft second heart sound
normally found in patients with aortic stenosis
202
what distinctive heart sound does pulmonary hypertension cause
a loud second heart sound as the pulmonary valve shuts hard
203
what is the treatment for torsades de pointes
IV magnesium
204
drug management of angina
* all patients should get aspirin and a statin unless contraindicated
* sublingual GTN PRN
* then a beta blocker OR calcium channel blocker
* if ccb monotherapy then rate limiter such as diltiazem or verapamil
* then b blocker and ccb dual therapy
* if using b blocker and ccb in combination then use nifedepine (remember that verapamil can't be used with beta blockers)
* then consider addition of long acting nitrite such as isosorbide mononitrate while they await assessment for PCI or CABG
205
what is the most common artery affected by peripheral arterial disease
femoral artery
206
how do you confirm a diagnosis of peripheral arterial disease
doppler ultrasonography
207
what are the different ABPI readings for different levels of limb ischaemia
1 = normal
0. 6-0.9 = claudication
0. 3-0.6 = rest pain
\<0.3 = impending gangrene
208
what are the principle risk factors for peripheral arterial disease
smoking and diabetes
209
management of intermittent claudication
* exercise (supervised programme if available)
* refer for consideration of angioplasty or bypass surgery
* antiplatelet therapy with aspirin or clopidogrel
210
what are the interventions for acute lower limb ischaemia
* endovascular therapies
* percutaneous catheter directed thrombolytic therapy
* percutaneous mechanical thrombus extraction
* surgical interventions
* endarterectomy
* bypass surgery
* surgical thromboembolectomy
* amputation if limb is unsalvageable
211
what is acute limb ischaemia
a sudden decrease in limb perfusion that threatens limb viability. In acute limb ischaemia, decreased perfusion and symptoms and signs develop over less than 2 weeks.
212
what most commonly causes acute limb ischaemia
a thrombosis within a diseased artery when a plaque ruptures
213
what is the definition of an abdominal aneurysm
an aortic diameter of 3 cm or greater
214
when would an unruptured AAA be repaired?
* if it is symptomatic
* if it is asymptomatic but larger than 4.0cm and has grown by more than 1cm in the last year
* if it is asymptomatic and 5.5cm or larger
215
what is the monitoring for AAA
* 3.0-4.4 cm: annual ultrasound.
* 4.5-5.4 cm: three-monthly ultrasound.
* 5.5 cm or bigger - consider surgery (see below): or three-monthly ultrasound.
216
how are AAAs repaired
* open surgical repair
* aortic and iliac clamping
* removal or aneurysmal segment
* replacement with a prosthetic graft
* endovascular repair of AAA (EVAR)
* stent graft system introduced through femoral arteries
217
what is AAA screening
screening by ultrasound for men aged 65 - if negative this rules out AAA for life
218
is AAA more common in men or women
it is 6 times more common in men
219
what are the specific causes of AAA
* Trauma.
* Infection - brucellosis, salmonellosis, tuberculosis, HIV.
* Inflammatory diseases - eg, Behçet's disease, Takayasu's disease. Inflammatory aneurysms may have multifactorial pathology[[5](https://patient.info/doctor/abdominal-aortic-aneurysms#ref-5)].
* Connective tissue disorders - Marfan's syndrome, Ehlers-Danlos syndrome type IV.
220
what are the causes of TAA
* Genetic
* In some families, there appears to be an autosomal dominant trait causing TAA
* Certain connective tissue disorders:
* Marfan's syndrome.
* Ehlers-Danlos syndrome type IV
* Infections:
* Tertiary syphilis
* Mycotic aneurysm[[8](https://patient.info/doctor/thoracic-aortic-aneurysms#ref-8)]
* HIV[[9](https://patient.info/doctor/thoracic-aortic-aneurysms#ref-9)]
* Aortitis
* giant cell arteritis
* rheumatoid arthritis
* Behçet's disease
* Takayasu's arteritis
* Trauma.
* Weightlifting, cocaine and amfetamine use
* perhaps because of the large rises in blood pressure which occur during these activities.
221
best imaging for AAA and TAA
CT scan with contrast as detailed views are needed for repair planning
222
who needs surgery for an unruptured TAA
* If it's symptomatic regardless of size then it needs surgery
* asumptomatic TAAs with diameter \>5.5 ascending aorta and \>6cm descending aorta
* patients with strong family history or marfans may need surgery sooner
223
what is the most common risk factor for aortic dissection
hypertension
224
what are the important features about the pain in aortic dissection
* pain is abrupt and maximal at onset unlike in MI
* pain migrates as dissection progresses
* proximal dissections - pain retrosternal
* distal dissections - pain between scapulae
* described as sharp, tearing and ripping
225
what is the secondary prevention of ACS
* patients who have had ACS require lifelong treatment to reduce risk of another event - this includes:
* aspirin
* clopidogrel
* beta blocker
* ace inhibitor
* staitin
226
what is the secondary prevention of ACS
* patients who have had ACS require lifelong treatment to reduce risk of another event - this includes:
* aspirin
* clopidogrel
* beta blocker
* ace inhibitor
* staitin
227
what are the stemi criteria
* clinical symptoms consistent with ACS ECG features in ≥ 2 contiguous leads of:
* ≥ 2.5 small squares ST elevation in leads V2-3 in men under 40 years, or ≥ 2 small squares ST elevation in leads V2-3 in men over 40 years
* 1.5 small square ST elevation in V2-3 in women
* 1 small square ST elevation in other leads
* new LBBB (LBBB should be considered new unless there is evidence otherwise)
228
what is stemi management
* notes
* it means if PCI is going to take longer than 120 minutes to organise then give fibrinolysis instead
* an ecg should be done 60-90 minutes after fibrinolysis and if they still have ST elevation then consider PCI
229
what is NSTEMI and ACS management
230
how do you assess risk of future cardiac events in patients with ACS
* GRACE score which uses the following factors
* age
* heart rate, blood pressure
* cardiac (Killip class) and renal function (serum creatinine)
* cardiac arrest on presentation
* ECG findings
* troponin levels
231
where is venous ulceration seen typically
above the medial malleolus
232
management of venous ulcers
* compression bandaging, usually four layer (only treatment shown to be of real benefit)
* oral pentoxifylline, a peripheral vasodilator, improves healing rate
233
what are the features of arterial ulcers
* Occur on the toes and heel
* Painful
* There may be areas of gangrene
* Cold with no palpable pulses
* Low ABPI measurements
234
are venous ulcers typically painful?
no typically painful
235
what is the inheritance pattern of haemochromatosis
AR
236
what gene is implicated in haemochromatosis
HFE - needs both copies to be mutated
237
presenting features of haemochromatosis
* early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)
* 'bronze' skin pigmentation
* diabetes mellitus
* liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
* cardiac failure (2nd to dilated cardiomyopathy)
* hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
* arthritis (especially of the hands)
238
which complications of haemochromatosis are reversible and which are non-reversible
239
what are the diagnostic tests for haemochromatosis
* liver biopsy - perl's stain
* molecular genetic testing
240
what would iron studies in someone with haemochromatosis be
* transferrin saturation \> 55% in men or \> 50% in women
* raised ferritin (e.g. \> 500 ug/l) and iron
* low TIBC
241
management of haemochromatosisq
* venesection is first line
* desferrioxamine as second line
242
what is the most common risk factor for infective endocarditis
previous episode of endocarditis
243
infective endocarditis in IVDUs typically affects which valve
tricuspid
244
most common causative organisms of infective endocarditis
* staphylococcus aureus - most common
* strep viridans - most common in developing world
245
culture negative causes of infective endocarditis
* prior antibiotic therapy
* *Coxiella burnetii*
* *Bartonella*
* *Brucella*
246
infective endocarditis can be diagnosed with what combination of the duke criteria
* pathological criteria positive, or
* 2 major criteria, or
* 1 major and 3 minor criteria, or
* 5 minor criteria
247
what are the pathological criteria of the duke criteria
Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)
248
what are the major criteria for duke criteria
* positive blood cultures
* two if organism specific for IE (such as strep viridans)
* three if less specific organism - must be taken 12 hrs apart
* evidence of endocardial involvement
* new valvular regurge
* positive echo
249
what are the minor criteria for duke criteria
* predisposing heart condition or intravenous drug use
* microbiological evidence does not meet major criteria
* fever \> 38ºC
* vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
* immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots
250
what is the initial blind therapy for infective endocarditis
* if native valve
* amoxicillin, consider adding low-dose gentamicin
* If penicillin allergic, MRSA or severe sepsis
* vancomycin + low-dose gentamicin
* If prosthetic valve
* vancomycin + rifampicin + low-dose gentamicin
251
what are the three types of ischaemia to the lower GI tract
* acute mesenteric ischaemia
* chronic mesenteric ischaemia
* ischaemic colitis
252
how do you diagnose bowel ischaemia
CT
253
What causes acute mesenteric ischaemia
embolism resulting in occlusion of an artery which supplies the small bowel - for example the superior mesenteric artery
patients classically have a history of AF
254
what is the management of acute mesenteric ischaemia
urgent surgery - poor prognosis if surgery's delayed
255
what is ischaemic colitis and why does it typically occur where it typically does
Ischaemic colitis describes an acute but transient compromise in the blood flow to the large bowel. This may lead to inflammation, ulceration and haemorrhage.
It is more likely to occur in 'watershed' areas such as the **splenic flexure** that are located at the borders of the territory supplied by the **superior and inferior mesenteric arteries.**
256
management for ischaemic colitis
* usually supportive
* surgery may be required in a minority of cases if conservative measures fail. Indications would include:
* generalised peritonitis,
* perforation or
* ongoing haemorrhage
257
causes of myocarditis
* viral: coxsackie B, HIV
* bacteria: diphtheria, clostridia
* spirochaetes: Lyme disease
* protozoa: Chagas' disease, toxoplasmosis
* autoimmune
* drugs: doxorubicin
258
what is the classic presentation of myocarditis
* usually young patient with an acute history
* chest pain
* dyspnoea
* arrhythmias
259
what will the bloods show in myocarditis
* ↑ inflammatory markers in 99%
* ↑ cardiac enzymes
* ↑ BNP
260
what is the management of myocarditis
* treatment of underlying cause e.g. antibiotics if bacterial cause
* supportive treatment e.g. of heart failure or arrhythmias
261
what are the complications of myocarditis
* heart failure
* arrhythmia, possibly leading to sudden death
* dilated cardiomyopathy: usually a late complication
262
what are the features of acute pericarditis
* chest pain: may be pleuritic. Is often relieved by sitting forwards
* other symptoms include non-productive cough, dyspnoea and flu-like symptoms
* pericardial rub
* tachypnoea
* tachycardia
263
what are the causes of pericarditis
* viral infections (Coxsackie)
* tuberculosis
* uraemia (causes 'fibrinous' pericarditis)
* trauma
* post-myocardial infarction, Dressler's syndrome
* connective tissue disease
* hypothyroidism
* malignancy
264
ECG changes of acute pericarditis
widespread saddle shaped st elevation
pr depression - most specific pericarditis marker
265
what is the management of pericarditis
treat cause if known
combination of NSAIDS and colchicine is now generally used to treat idiopathic or viral pericarditis
266
which is a cause of pericarditis that is most likely to cause constrictive pericarditis
TB
