Cardiology Flashcards
what is the MOA of ACEi
inhibits conversion of angiotensin 1 to II - causes vasodilation and reduced blood pressure // reduces stimulation for aldosterone release decreasing socium and water retention by the kidneys
ACEi - dilate efferent arterioles, reduce glomerular capillary pressure
monitor urea and electrolytes before treatment is initiated and after increasing the dose
side effects and contra-indications of ACE inhibitors
cough
angioedema
hyperkalaemia
first-dose hypotension
C/I
pregnancy and breastfeeding
renovascular disease
aortic stenosis - may cause hypotension
patients with high dose diuretic therapy
causes of acute pericarditis
viral infections (Coxsackie)
tuberculosis
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
features of acute pericarditis
inflammation of pericardial sac for <4-6w
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
what are some findings in acute pericarditis
ECG changes
PR depression
global/widespread saddle-shaped ST elevation
transthoracic echocardiography
bloods
inflammatory markers
troponin: around 30% of patients may have an elevated troponin - this indicates possible myopericarditis
management of acute pericarditis
IPT mx if high risk features - fever >38, elevated troponin
otherwise OPT
treat underlying cause
avoid strenuous activity until sx resolution
1st line - NSAIDs and colchicine
indications for adenosine
termination of supraventricular tachycardia by causing transient heart block in AVN
effects enhanced by dipuridamole (antiplatelet) and blocked by theophyllines
adverse effects: chest pain, bronchospasm, transient flushing
adult ALS - non-shockable rhythms
non-shockable rhythms - asystole, PEA
adrenaline 1mg ASAP
repeat adrenaline 1mg every 3-5mins
chest compressins 30:2
give thrombolysis if PE suspected
adult ALS - shockable rhythms
VF/pulseless VT
chest compressions 30:2
single shock + 2 mins CPR
(if cardiac arrest witnessed - 3 stacked shocks then CPR)
adrenaline 1mg after 3 shocks, repeat 3-5min
amiodarone 300mg after 3 shocks, amiodarone 150mg after 5 shocks (lidocaine if unavailable)
give thrombolysis if PE suspected
reversible causes of cardiac arrest
Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade – cardiac
Toxins
when to use amiodarone
amiodarone is class III antiarrhythmic agent to treat atrial, nodal and ventricular tachycardias
give into central veins
may cause arrhythmia due to prolongation of QT interval
adverse effects of amiodarone
thyroid dysfunction: both hypothyroidism and hyper-thyroidism
corneal deposits
pulmonary fibrosis/pneumonitis
liver fibrosis/hepatitis
peripheral neuropathy, myopathy
photosensitivity
‘slate-grey’ appearance
thrombophlebitis and injection site reactions
bradycardia
lengths QT interval
drug management of angina pectoris
aspirin and statin
sublingual glyceryl trinitrate to abort angina attacks
beta-blocker or CCB
if CCB monotherapy - use rate limiting (verapamil, diltiazem)
+ both
+ 3rd drug whilst patient is awaiting assessment for PCI or CABG
when to use antiplatelets
ACS - lifelong aspirin, 12month ticagrelor
PCI - lifelong aspirin and 12m prasugrel/ticagrelor
TIA - lifelong clopidogrel
ischaemic stroke - lifelong clopidogrel
peripheral arterial disease - lifelong clopidogrel
what are the features of aortic dissection
tear in the tunica intima of the wall of the aorta
features:
sharp tearing chest/back pain
pulse deficit - weak/absent carotid, brachial, or femoral pulse
aortic regurgitation
hypertension
what is aortic dissection associated with
hypertension: the most important risk factor
trauma
bicuspid aortic valve
collagens: Marfan’s syndrome, Ehlers-Danlos syndrome
Turner’s and Noonan’s syndrome
pregnancy
syphilis
classifications of aortic dissection
Stanford classification
type A - ascending aorta, 2/3 of cases
type B - descending aorta, distal to left subclavian origin, 1/3 of cases
DeBakey classification
type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
type II - originates in and is confined to the ascending aorta
type III - originates in descending aorta, rarely extends proximally but will extend distally
investigation of aortic dissection
Chest x-ray
widened mediastinum
CT angiography CAP - for stable patients and for planning surgery
false lumen = aortic dissection
Transoesophageal echocardiography (TOE)
more suitable for unstable patients who are too risky to take to CT scanner
management of aortic dissection
Type A
surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention
Type B*
conservative management
bed rest
reduce blood pressure IV labetalol to prevent progression
chronic causes of aortic regurgitation
due to valve disease:
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)
aortic root disease:
bicuspid aortic valve (affects both the valves and the aortic root)
spondylarthropathies (e.g. ankylosing spondylitis)
hypertension
syphilis
Marfan’s, Ehler-Danlos syndrome
acute causes of aortic regurgitation
infective endocarditis
aortic dissection
features of aortic regurgiation
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
how is aortic regurgitation managed
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
clinical features of 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
this is decreased following the Valsalva manoeuvre
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
causes of aortic stenosis
degenerative calcification (most common cause in older patients > 65 years)
bicuspid aortic valve (most common cause in younger patients < 65 years)
William’s syndrome (supravalvular aortic stenosis)
post-rheumatic disease
subvalvular: HOCM
managing aortic stenosis
asymtpomatic - observe
symptomatic - valve replacement
asymptomatic but valvular gradient >40 - consider surgery
options for AVR
surgical AVR is the treatment of choice for young, low/medium operative risk patients
transcatheter AVR (TAVR) is used for patients with a high operative risk
balloon valvuloplasty - used in children with no aortic valve calcification
what is arrhythmogenic right ventricular cardiomyopathy
inherited CVD presenting with syncope or sudden cardiac death (2nd after HOCM)
AD inheritance, right ventricular myocardium replaced by fatty and fibrofatty tissue
features of arrhythmogenic right ventricular cardiomyopathy
presents with palpitations, syncope, and sudden cardiac death
ECG abnormalities in V1-3, T wave inversion
50% pt have an episilon wave (terminal notch)
echo - enlarged hypokinetic right ventricle with thin free wall
management of arrhythmogenic right ventricular cardiomyopathy
drugs - sotalol
catheter ablation - prevent ventricular tachycardia
implantable cardioverter defibrillator
definition and types of atrial fibrillation
most common sustained cardiac arrhythmia
first detected episode - irrespective of symptomatic or self-terminating
recurrent episodes - >2 episodes
if terminates spontaneously - paroxysmal AF (episodes last <7 days)
if non-self terminating - persistent AF
permanent AF - continuous AF cannot be cardioverted
features of atrial fibrillation
Symptoms
palpitations
dyspnoea
chest pain
Signs
an irregularly irregular pulse
ECG - absent p waves and irregularly irregular QRS complexes
rate management of atrial fibrillation
beta blocker or a rate limiting calcium channel blocker (diltiazem)
offer if <48h, start rate control if >48h
rhythm management of atrial fibrillation
offer if onset <48h
e.g., digoxin
risk of stroke when restored to sinus rhythm - therefore need to have short sx duration <48h or be anticoagulated for a period of time before attempting cardioversion
how to use the CHA2DS2-VASc score
congestive heart failure
hypertension
age >75
diabetes
prior stroke, TIA or thromboembolism
vascular disease disease
sex
score 0 - no treatment
score 1 - consider anticoagulation
score 2 - offer anticoagulation
anticoagulation in AF
assess need for anticoagulation - CHADs2 VASc
assess bleeding risk - ORBIT score
DOACs
apixaban
dabigatran
edoxaban
rivaroxaban
warfarin - second line
how is cardioversion used in atrial fibrillation
emergency electrical cardioversion when pt is haemodynamically unstable
elective electrical/pharmacological cardioversion when rhythm control strategy is preferred
if AF <48h - heparinise
cardiovert using electrical DC cardioversion or amiodarone
if AF >48h - 3w anticoagulation prior to cardioversion then 4w anticoagulation
what drugs are used in pharmacological cardioversion
amiodarone
flecainide - if no structural heart disease
treatment of AF post-stroke
long term stroke prevention - warfarin or direct thrombin inhibitor or fXa inhibitor (apixaban)
start anticoag immediately after TIA
start after 2w if acute stroke, with antiplatelet therapy in interim
when is catheter ablation used in AF
used when poor response to antiarrhythmic medication
anticoagulate 4 weeks before and during procedure
what is atrial flutter + ECG findings
supraventricular tachycardia - rapid atrial depolarisation waves
ECG - sawtooth appearance
atrial rate 300/min
ventricular (HR) based on degree of AV block - e.g., 2:1 block = 150/min ventricular rate
how is atrial flutter managed
managed similar to AF (medication may be less effective)
more sensitive to cardioversion
radiofrequency ablation of tricuspid valve isthmus - curative
features of atrial myxoma
most common primary cardiac tumour, occurs in left atrium and in F
Features
systemic: dyspnoea, fatigue, weight loss, pyrexia of unknown origin, clubbing
emboli
atrial fibrillation
mid-diastolic murmur, ‘tumour plop’
echo: pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum
what are the recognised atrial septal defects and their features
ASF - most likely congenital heart defect in adulthood
Features
ejection systolic murmur, fixed splitting of S2
embolism may pass from venous system to left side of heart causing a stroke
ostium secundum (70% ASDs)
assx Holt Oram syndrome (tri-phalangeal thumbs)
ECG: RBBB with RAD
ostium primum
presents earlier
abnormal AV valves
ECG: RBBB with LAD, prolonged PR interval
what are the types of atriventricular block
AV block = impaired electrical conduction between atria and ventricular
1st degree heart block - PR >0.2s
2nd degree heart block - type 1 - prolongation of PR interval until dropped beat
type 2 - PR constant but P wave not often followed by QRS
third degree - complete
no association between P waves and QRS
what is B-type natriuretic peptide
BNP - hormone produced mainly by left ventricular myocardium in response to strain that causes vasodilation, diuretic and natriuretic, suppresses SNS and RAAS
raised levels may be caused by - reduced excretion in CKS, myocardial ischaemia, valvular disease
what are the uses of BNP
diagnosing patients with acute dyspnoea
ruling out heart failure
prognosis in chronic heart failure
guiding treatment in chronic heart failure
some indications for beta blockers
angina
post-myocardial infarction
heart failure: beta-blockers were previously avoided in heart failure but there is now strong evidence that certain beta-blockers improve both symptoms and mortality
arrhythmias: beta-blockers have now replaced digoxin as the rate-control drug of choice in atrial fibrillation
hypertension: the role of beta-blockers has diminished in recent years due to a lack of evidence in terms of reducing stroke and myocardial infarction.
thyrotoxicosis
migraine prophylaxis
anxiety
some side effects of beta blockers
bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction
contra-indications for beta-blockers
uncontrolled heart failure
asthma
sick sinus syndrome
concurrent verapamil use: may precipitate severe bradycardia
uses of direct thrombin inhibitors
Bivalirudin is a reversible direct thrombin inhibitor used as an anticoagulant in the management of acute coronary syndrome.
features of broad complex tachycardias
ventricular tachycardias
Features suggesting VT rather than SVT with aberrant conduction
AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 ms
what is brugada syndrome
autosomal dominant CVS disease causing sudden cardiac death
managed with implantable cardioverter defibrillator
what are the ECG changes seen in brugada syndrome
partial RBBB
convex ST elevation V1-V3 followed by negative T wave
what are the features of buerger’s disease (thromboangiitis obliterans)
small and medium vessel vasculitis assx with smoking
Features
extremity ischaemia
intermittent claudication
ischaemic ulcers
superficial thrombophlebitis
Raynaud’s phenomenon
normal oxygen saturation levels seen in cardiac catheterisation
IVC/SVC - 70%
RA, RV, PA - 70%
lungs oxygenate blood to 98-100% - LA, LV should saturate 98-100%
what are the time frames for cardiac enzymes
myoglobin - rises 1-2h, peaks 6-8h
CK - 4-8h, peaks 16-24h
trop T - rises 4-6h, peaks 12-24h
what are the differences between troponin I and T
troponin I - unique to heart muscle
troponin T - troponin T exists in other types of muscle
troponin levels increase 3-12h after heart attack
features of cardiac tamponade
cardiac tamponade - accumulation of pericardial fluid under pressure
Beck’s triad:
hypotension
raised JVP
muffled heart sounds
dyspnoea
tachycardia
an absent Y descent on the JVP - this is due to the limited right ventricular filling
pulsus paradoxus - an abnormally large drop in BP during inspiration
Kussmaul’s sign - much debate about this
ECG: electrical alternans
management for cardiac tamponade
urgent pericardiocentesis
features of hypertrophic obstructive cardiomyopathy
Leading cause of sudden cardiac death in young athletes
Usually due to a mutation in the gene encoding β-myosin heavy chain protein
Common cause of sudden death
Echo findings include MR, systolic anterior motion (SAM) of the anterior mitral valve and asymmetric septal hypertrophy
causes of dilated cardiomyopathy
Classic causes include
alcohol
Coxsackie B virus
wet beri beri
doxorubicin
causes of restrictive cardiomyopathy
Classic causes include
amyloidosis
post-radiotherapy
Loeffler’s endocarditis
types of acquired cardiomyopathy
peripartum cardiomyopathy
typical develops between last month of pregnancy and 5 months post-partum
More common in older women, greater parity and multiple gestations
takotsubo cardiomyopathy
‘Stress’-induced cardiomyopathy e.g. patient just found out family member dies then develops chest pain and features of heart failure
Transient, apical ballooning of the myocardium
Treatment is supportive
causes of chest pain
aortic dissection
pulmonary embolism
myocardial infarction
perforated peptic ulcer
boerhaaves syndrome
drug therapy guidelines for chronic heart failure
1 - ACEi, beta-blocker
2 - aldosterone antagonist
SGLT-2 inhibitors
3 - ivabradine, sacubitril valsartan, digoxin, hydralazine, cardiac resynchronisation therapy
offer annual influenza vaccine
one off pneumococcal vaccine
NYHA classification of chronic heart failure
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
features of coarctation of aorta
infancy: heart failure
adult: hypertension
radio-femoral delay
mid systolic murmur, maximal over the back
apical click from the aortic valve
notching of the inferior border of the ribs (due to collateral vessels) is not seen in young childre
features of complete heart block
heart failure
regular bradycardia (30-50 bpm)
wide pulse pressure
JVP: cannon waves in neck
variable intensity of S1
causes and features of constrictive pericarditis
causes - any cause of pericarditis, TB
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
CXR - pericardial calcification
hypertension management in diabetes mellitus
DM patients need strict BP control to reduce overall cardiovascular risk
BP targets for intervention should be 135/85 mmHg or 130/80mmHg if albuminuria or >2 features of metabolic
ACEi or A2RBs - regardless of age
causes of dilated cardiomyopathy
most common form of cardiomyopathy
idiopathic: the most common cause
myocarditis: e.g. Coxsackie B, HIV, diphtheria, Chagas disease
ischaemic heart disease
peripartum
hypertension
iatrogenic: e.g. doxorubicin
substance abuse: e.g. alcohol, cocaine
inherited: either a familial genetic predisposition to DCM or a specific syndrome e.g. Duchenne muscular dystrophy
around a third of patients with DCM are thought to have a genetic predisposition
a large number of heterogeneous defects have been identified
the majority of defects are inherited in an autosomal dominant fashion although other patterns of inheritance are seen
infiltrative e.g. haemochromatosis, sarcoidosis
features of dilated cardiomyopathy
classic findings of heart failure
systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
S3
‘balloon’ appearance of the heart on the chest x-ray
dilated heart leading to predominately systolic dysfunction
all 4 chambers are dilated, but the left ventricle more so than right ventricle
eccentric hypertrophy (sarcomeres added in series) is seen
specific rules for CVS disorders RE DVLA
hypertension - can drive unless unacceptable S/E
CABG - 4 weeks off
ACS - 4 weeks off
angina - driving must cease if sx occur at rest
pacemaker - 1 week off
implantable cardioverter defibrillator - for ventricular arrhythmia cease driving for 6m, prophylactically implanted, cease driving for 1m
aortic aneurysm - notify DVLA
ECG: atrial and ventricular hypertrophy signs
LVH - S wave (V1) + R wave (V5/V6) exceeds 40mm
RVH
LA enlargement - bifid p wave lead II >120ms
RA enlargement - tall p waves in lead II and V1
causes of left axis deviation
left anterior hemiblock
left bundle branch block
inferior myocardial infarction
Wolff-Parkinson-White syndrome* - right-sided accessory pathway
hyperkalaemia
congenital: ostium primum ASD, tricuspid atresia
minor LAD in obese people
causes of right axis deviation
right ventricular hypertrophy
left posterior hemiblock
lateral myocardial infarction
chronic lung disease → cor pulmonale
pulmonary embolism
ostium secundum ASD
Wolff-Parkinson-White syndrome* - left-sided accessory pathway
normal in infant < 1 years old
minor RAD in tall people
bi-fascicular block vs trifascicular block on ECG
bi-fascicular block - RBBB with LAD
trifascicular block - bifascicular block + 1st degree HB
coronary territories on ECG
anteroseptal - V1-V4
inferior - II, III, aVF
anterolateral - V1-6, I, aVL
lateral - I, aVL, V5, V6
posterior - changes in V1-3, reciprocal changes of STEMI
ECG signs of digoxin toxicity
down-sloping ST depression (‘reverse tick’, ‘scooped out’)
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia
ECG features of hypokalaemia
U waves
small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT
ECG features of hypothermia
bradycardia
‘J’ wave (Osborne waves) - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias
LBBB and RBBB on ECG
MaRRoW
in LBBB there is a ‘W’ in V1 and a ‘M’ in V6
in RBBB there is a ‘M’ in V1 and a ‘W’ in V6
ECG changes on acute myocardial infarction
hyperacute T waves - for a few minutes
ST elevation
T waves become inverted <24 hours - lasting days - months
pathological Q waves develop after several hours to days
ECG definition of 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)
some normal variants in ECG
sinus bradycardia
junctional rhythm
first degree heart block
Mobitz type 1 (Wenckebach phenomenon)
causes of a prolonged PR interval on ECG
idiopathic
ischaemic heart disease
digoxin toxicity
hypokalaemia*
rheumatic fever
aortic root pathology e.g. abscess secondary to endocarditis
Lyme disease
sarcoidosis
myotonic dystrophy
causes of ST depression on ECG
secondary to abnormal QRS (LVH, LBBB, RBBB)
ischaemia
digoxin
hypokalaemia
syndrome X
causes of ST elevation on ECG
myocardial infarction
pericarditis/myocarditis
normal variant - ‘high take-off’
left ventricular aneurysm
Prinzmetal’s angina (coronary artery spasm)
Takotsubo cardiomyopathy
rare: subarachnoid haemorrhage
causes of inverted T waves
myocardial ischaemia
digoxin toxicity
subarachnoid haemorrhage
arrhythmogenic right ventricular cardiomyopathy
pulmonary embolism (‘S1Q3T3’)
Brugada syndrome
what is wellen’s syndrome
ECG pattern caused by high-grade stenosis in LAD coronary artery
ECG features
biphasic or deep T wave inversion in V2-3
minimal ST elevation
no Q waves
what is eisenmenger’s syndrome
reversal of left to right shunt in congenital heart defect due to pulmonary hypertension
uncorrected shunt leads to remodelling of pulmonary microvasculature, causes obstruction to pulmonary blood and pulmonary hypertension
features of eisenmenger’s syndrome
Features
original murmur may disappear
cyanosis
clubbing
right ventricular failure
haemoptysis, embolism
associations - ventricular septal defect, atrial septal defect, patent ductus arteriosus
managed by heart-lung transplantation
definition of acute heart failure
sudden onset or worsening of the symptoms of heart failure
AHF without a past history of heart failure is called de-novo AHF. Decompensated AHF is more common (66-75%) and presents with a background history of HF.
causes of de-novo heart failure
caused by increased cardiac filling pressures and myocardial dysfunction usually as a result of ischaemia
Causes reduced cardiac output and therefore hypoperfusion - can cause pulmonary oedema.
less common causes of de-novo AHF are:
Viral myopathy
Toxins
Valve dysfunction
causes of decompensated heart failure
Acute coronary syndrome
Hypertensive crisis
Acute arrhythmia
Valvular disease
There is generally a history of pre-existing cardiomyopathy. It usually presents with signs of fluid congestion, weight gain, orthopnoea and breathlessness.
classification of heart failure symptoms
With or without hypoperfusion
With or without fluid congestion
signs and symptoms of acute heart failure
symptoms - breathlessness, reduced exercise tolerance, oedema, fatigue
signs - cyanosis, tachycardia, elevated JVP, displaced apex beat, chest signs (bibasal crackles but may also cause wheeze), S3 heart sound
investigations for patients with acute heart failure
bloods - any underlying abnormalities (anaemia, abnormality, abnormality electrolytes, infection)
chest x-ray - pulmonary venous congestion, interstitial oedema, cardiomegaly
echo - for new onset HF and for patients with known HF with change in heart function
BNP - raised levels indicate myocardial damage
features of chronic heart failure
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
acute management of heart failure
recommended for all patients - IV loop diuretics (furosemide)
additional treatments - oxygen (94-98%), vasodilators
if respiratory failure - CPAP
if hypotensive - inotropic agents, vasopressor agents, mechanical criculatory assistance
opiates
what are the types of heart failure classification
by ejection fraction
by time
by left/right
by high/low output
types of ejection fraction issues in heart failure
reduced LVEF - <35-40% - HF-rEF
preserved LVEF - HF-pEF
systolic dysfunction
Ischaemic heart disease
Dilated cardiomyopathy
Myocarditis
Arrhythmias
diastolic dysfunction
Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis
left sided heart failure
typically develops left sided heart failure due to increased left ventricular afterload (arterial hypertension or aortic stenosis) or increased left ventricular preload (aortic regurgitation resulting in backflow to the left ventricle)
left ventricular failure results in:
pulmonary oedema
dyspnoea
orthopnoea
paroxysmal nocturnal dyspnoea
bibasal fine crackles
right sided heart failure
Right-sided heart failure is caused by either increased right ventricular afterload (e.g. pulmonary hypertension) or increased right ventricular preload (e.g. tricuspid regurgitation).
Right ventricular failure typically results in:
peripheral oedema
ankle/sacral oedema
raised jugular venous pressure
hepatomegaly
weight gain due to fluid retention
anorexia (‘cardiac cachexia’)
high-output heart failure
high output heart failure refers to a situation where a ‘normal’ heart is unable to pump enough blood to meet the metabolic needs of the body.
Causes
anaemia
arteriovenous malformation
Paget’s disease
Pregnancy
thyrotoxicosis
thiamine deficiency (wet Beri-Beri)
what are the heart sounds
S1 - closure of mitral and
S2 - closure of aortic and pulmonary valves
soft in aortic stenosis
S3 - diastolic filling of ventricle
heard in left ventricular failure, constrictive pericarditis
S4 - heard in aortic stenosis, HOCM, HTN, caused by atrial contraction against a stiff ventricle
causes of loud S1
mitral stenosis
left-to-right shunts
short PR interval, atrial premature beats
hyperdynamic states
causes of quiet S1
mitral regurgitation
causes of loud S2
hypertension: systemic (loud A2) or pulmonary (loud P2)
hyperdynamic states
atrial septal defect without pulmonary hypertension
causes of soft S2
aortic stenosis
Causes of fixed split S2
atrial septal defect
Causes of a widely split S2
deep inspiration
RBBB
pulmonary stenosis
severe mitral regurgitation
features of hypercalcaemia
‘bones, stones, groans and psychic moans’
corneal calcification
shortened QT interval on ECG
hypertension
types of xanthoma seen in hyperlipidaemia
Palmar xanthoma
remnant hyperlipidaemia
may less commonly be seen in familial hypercholesterolaemia
Eruptive xanthoma are due to high triglyceride levels and present as multiple red/yellow vesicles on the extensor surfaces (e.g. elbows, knees)
(caused by familial hypertriglyceridaemia, lipoprotein lipase deficiency)
Tendon xanthoma, tuberous xanthoma, xanthelasma
(caused by familial hypercholesterolaemia, remnant hyperlipidaemia)
what are xanthelasma
Xanthelasma are yellowish papules and plaques caused by localized accumulation of lipid deposits commonly seen on the eyelid. They are also seen in patients without lipid abnormalities.
definition of hypertension
a clinic reading persistently above >= 140/90 mmHg, or:
a 24 hour blood pressure average reading >= 135/85 mmHg
causes of hypertension
primary (essential)
secondary - secondary to endocrine, renal, other causes
- Glomerulonephritis
- Chronic pyelonephritis
- Adult polycystic kidney disease
- Renal artery stenosis
- Primary hyperaldosteronism
- Phaeochromocytoma
- Cushing’s syndrome
- Liddle’s syndrome
- Congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
- Acromegaly
- Glucocorticoids
- NSAIDs
- Pregnancy
- Coarctation of the aorta
- Combined oral contraceptive pill
symptoms and screening of HTN
if severely raised: headaches
visual disturbance
seizures
check for end organ damage
fundoscopy: to check for hypertensive retinopathy
urine dipstick: to check for renal disease, either as a cause or consequence of hypertension
ECG: to check for left ventricular hypertrophy or ischaemic heart disease
diagnosis and testing in hypertension
24 hour blood pressure
urea and electrolytes: check for renal disease, either as a cause or consequence of hypertension
HbA1c: check for co-existing diabetes mellitus, another important risk factor for cardiovascular disease
lipids: check for hyperlipidaemia, again another important risk factor for cardiovascular disease
ECG
urine dipstick
management of hypertension
ACEi - first line if <55, avoid if pregnant, check renal function after starting
CCB - first line if >55y or AC pt
Thiazide type diuretics
A2RB - used if ACEi are not tolerated
stages of hypertension
Stage 1 hypertension Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
Stage 2 hypertension Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
Severe hypertension Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg
managing high readings
If the difference in readings between arms is more than 20 mmHg then the measurements should be repeated.
take a second reading during the consultation, if the first reading is > 140/90 mmHg
offer ABPM or HBPM to any patient with a blood pressure >= 140/90 mmHg.
If the blood pressure is >= 180/120 mmHg refer to specialists if signs of organ damage or life-threatening symptoms, phaeo?, and request urgent ix for end organ damage
how is ambulatory BP monitoring used
Ambulatory blood pressure monitoring (ABPM)
at least 2 measurements per hour during the person’s usual waking hours (for example, between 08:00 and 22:00)
use the average value of at least 14 measurements
ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension)
treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 10% or greater
ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension)
offer drug treatment regardless of age
features of hypertrophic obstructive cardiomyopathy
autosomal dominant disorder of muscle tissue due to defective contractile proteins - causes death in young
causes diastolic dysfunction: LVH -> poor compliance, reduced CO
often asymptomatic
exertional dyspnoea
angina
syncope following exercise (subaortic hypertrophy of the ventricular septum results in functional aortic stenosis)
sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure
jerky pulse, large ‘a’ waves, double apex beat
systolic murmurs
echo findings in HOCM
MR SAM ASH
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)
ECG findings in HOCM
left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
atrial fibrillation may occasionally be seen
management of HOCM
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*
definition and cause of hypothermia
Mild hypothermia: 32-35°C
Moderate or severe hypothermia: < 32°C
Exposure to cold in the environment is the major cause
Inadequate insulation in the operating room
Cardiopulmonary bypass
Newborn babies.
Risk factors:
General anaesthesia
Substance abuse
Hypothyroidism
Impaired mental status
Homelessness
Extremes of age
signs of hypothermia
shivering
cold and pale skin. Frostbite occurs when the skin and subcutaneous tissue freeze, causing damage to cells.
slurred speech
tachypnoea, tachycardia and hypertension (if mild)
respiratory depression, bradycardia and hypothermia (if moderate)
confusion/ impaired mental state
how to investigate hypothermia
Temperature
12 lead ECG - acute ST-elevation and J waves or Osborn waves may appear
FBC, serum electrolytes. Haemoglobin and haematocrit can be elevated (due to haemoconcentration)
Blood glucose
Arterial blood gas
Coagulation factors
Chest X-ray
managing hypothermia
Initial management includes:
Removing the patient from the cold environment and removing any wet/cold clothing,
Warming the body with blankets
Securing the airway and monitoring breathing,
If the patient is not responding well to passive warming, you may consider maintaining circulation using warm IV fluids or applying forced warm air directly to the patient’s body
+ rapid re-warming can lead to peripheral vasodilation and shock
risk factors for infective endocarditis
previous episode of endocarditis
if prev normal valves - affects mitral valve
rheumatic valve disease (30%)
prosthetic valves
congenital heart defects
intravenous drug users (IVDUs) - will cause tricuspid lesion
causative organisms for infective endocarditis
staphylococcus aureus - most common cause, common in acute presentation and IVDU
streptococcus viridans - poor dental hygiene
staphylococcus epidermidis (coagulase negative) - indwelling lines, post-surgery
major and minor criteria in modified duke criteria
diagnosis of infective endocarditis if:
pathological criteria positive // 2 major criteria // 1 major and 3 minor criteria // 5 minor criteria
major - positive blood cultures, persistent bacteraemia, positive serology, evidence of endocardial involvement
minor - previous heart condition, microbial evidence, >38C, vascular phenomena, immunological phenomena
management of infective endocarditis
initial therapy
amoxicillin (+gent) if native valve
if C/I, MRSA or sepsis - vancomycin + gent
vancomycin + rifampicin + gent if prosthetic valve
if native + staph - flucloxicillin
prosthetic + staph - flucloxacillin + rifampicin + gent
if strep - benzylpenicillin
if penallergic - vanc + gent
investigations indicated in patient with palpitations
12 lead ECG
TFTs
U+Es
FBC
Holter monitoring - continuously records ECG from 2-3 leads for 24h
what is isolated systolic hypertension
common in elderly - treat with same stepwise fashion as standard HTN
what is ivabradine
Ivabradine is a class of anti-anginal drug which works by reducing the heart rate. It acts on the If (‘funny’) ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity.
Adverse effects
visual effects, particular luminous phenomena, are common
headache
bradycardia, heart block
what are the JVP waves
a wave - atrial contraction
cannon a wave - atrial contraction against closed tricuspid
c wave - closure of tricuspid
v wave - passive filling in atrium against closed tricuspid
y descent - opening of tricuspid
what is long QT syndrome
delayed repolarization of the ventricles, may lead to ventricular tachycardia/torsade de pointes, can cause sudden death
causes of long QT
congenital
drugs
amiodarone, sotalol, class 1a antiarrhythmic drugs
TCAs, SSRIs, erythromycin, haloperidolm ondansetron
other
hypocalcaemia/kalaemia/magnesaemia
acute MI
myocarditis
hypothermia
SAH
use of loop diuretics and examples
Furosemide and bumetanide - inhibit the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl
indication:
heart failure: both acute (usually intravenously) and chronic (usually orally)
resistant hypertension, particularly in patients with renal impairment
features of mitral regurgitation
occurs when blood leaks back through the mitral valve on systole
can cause the myocardium to thicken over time -> fatigue and heart failure
usually asymptomatic
may have left ventricle failure symptoms
pansystolic blowing murmur, loudest at apex, radiates into axilla
causes of mitral regurgitation
post MI
mitral valve prolapse
infective endocarditis
rheumatic fever
congenital
treatment of mitral regurgitation
acutely, nitrates, diuretics, positive inotropes - to increase CO
if HF - ACEi and BB and spironolactone
if severe - surgery
features of mitral stenosis
obstruction of blood flow across the mitral valve from the left atrium to the left ventricle - leads to increases in pressure within the left atrium, pulmonary vasculature and right side of the heart.
dyspnoea, haemoptysis
mid-late diastolic murmur
loud SI
opening snap
malar flush
management of mitral stenosis
if assx with AF - anticoagulation with warfarin or DOAC
if asymptomatic - regular echo
if symptomatic - percutaneous mitral balloon valvotomy, mitral valve surgery
features of mitral valve prolapse
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
features and causes of ejection systolic murmur
if louder on expiration - aortic stenosis, hypertrophic obstructive cardiomyopathy
if louder on inspiration - pulmonary stenosis,
atrial septal defect
also: tetralogy of Fallot
features and causes of pansystolic murmur
mitral/tricuspid regurgitation (high-pitched and ‘blowing’ in character)
tricuspid regurgitation becomes louder during inspiration, unlike mitral reguritation
during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole
ventricular septal defect (‘harsh’ in character)
features and causes of late systolic murmur
mitral valve prolapse
coarctation of aorta
features and causes of early diastolic murmur
aortic regurgitation (high-pitched and ‘blowing’ in character)
Graham-Steel murmur (pulmonary regurgitation, again high-pitched and ‘blowing’ in character)
features and causes of mid-late diastolic murmur
mitral stenosis (‘rumbling’ in character)
Austin-Flint murmur (severe aortic regurgitation, again is ‘rumbling’ in character)
what is RILE
Right-sided murmur → heard best on Inspiration
Left-sided murmur → heard best on Expiration
some complications of MI
cardiac arrest
cardiogenic shock
chronic heart failure
tachyarrhythmias
bradyarrhythmias
pericarditis
left ventricular aneurysm
left ventricular free wall rupture
ventricular septal defect
acute mitral regurgitation
drugs used in the secondary prevention of MI
dual antiplatelet therapy (aspirin plus a second antiplatelet agent - ticagrelor and prasugrel)
ACE inhibitor
beta-blocker
statin
if acute MI and sx of heart failure or LV systolic dysfunction, treat with aldosterone antagonist post MI
acute management of a STEMI
aspirin 300mg
ticagrelor or prasugrel (if PCI)
unfractionated heparin (if PCI)
PCI - gold standard
if no access to PCI <2h - thrombolysis with tissue plasminogen activator (-plase)
ECG 90mins after thrombolysis to assess if 50% resolution - if not, rescue PCI
causes of myocarditis
viral: coxsackie B, HIV
bacteria: diphtheria, clostridia
spirochaetes: Lyme disease
protozoa: Chagas’ disease, toxoplasmosis
autoimmune
drugs: doxorubicin
presentation and features of myocarditis
inflammation of the myocardium
Presentation
usually young patient with an acute history
chest pain
dyspnoea
arrhythmias
bloods - inflammatory markers++, cardiac enzymes++, BNP++
ECG - tachycardia, arrhythmia, ST/T wave changes
management of myocarditis
treat underlying cause
supportive treatment
uses and effects of nicorandil
vasodilatory drug used to treat angina
potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.
dverse effects
headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration
uses and effects of nitrates
vasodilators used in angina and acute mx of HF
nitrates cause the release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels
in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand
Side-effects
hypotension
tachycardia
headaches
flushing
features and causes of orthostatic hypotension
Orthostatic hypotension is more common in older people and patients who have neurodegenerative disease (e.g. Parkinson’s) diabetes, or hypertension
Iatrogenic causes include alpha-blockers (e.g. for benign prostatic hyperplasia).
Features
a drop in BP (usually >20/10 mm Hg) within three minutes of standing
presyncope
syncope
managing orthostatic hypotension
treatment options include midodrine and fludrocortisone
indications for temporary pacemaker
symptomatic/haemodynamically unstable bradycardia, not responding to atropine
post-ANTERIOR MI: type 2 or complete heart block
post-INFERIOR MI complete heart block is common and can be managed conservatively if asymptomatic and haemodynamically stable
trifascicular block prior to surgery
indications and examples of parenteral anticoagulation
used for the prevention of venous thromboembolism and in the management of acute coronary syndrome
unfractionated heparin
LMWH
fondaparinux SC - activates antithrombin III, inhibits coagulation factors Xa
direct thrombin inhibitors - bivalirudin IV
adverse signs in peri-arrest bradycardia (requiring treatment)
shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
syncope
myocardial ischaemia
heart failure
treatment of peri-arrest bradycardia
atropine 500mcg IV (up to maximum 3mg)
transcutaneous pacing
isoprenaline/adrenaline infusion
there is potential risk of asystole
adverse signs in peri-arrest tachycardia (requiring treatment)
shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
syncope
myocardial ischaemia
heart failure
treatment of peri-arrest tachycardia
synchronised DC shocks - up to 3 then expert help
broad complex - assume ventricular, give loading dose amiodarone then 24h infusion
broad irregular - seek expert help
narrow complex - vagal manouvres, IV adenosine
narrow irregular - ?AF, consider chemical cardioversion or BB
causes and definition of postural hypotension
Postural hypotension may be defined as a fall of systolic blood pressure > 20 mmHg on standing.
Causes
hypovolaemia
autonomic dysfunction: diabetes, Parkinson’s
drugs: diuretics, antihypertensives, L-dopa, phenothiazines, antidepressants, sedatives
alcohol
features of premature ventricular complexes/beats
beats originating in the ventricular myocardium - common, idiopathic (may be due to HTN or MI)
usually asymptomatic
palpitations, irregular pulse
ECG - wide QRS
management of patients with biological valves
will structurally deteriorate and calcify over time - given to pt >65y
warfarin for 3m
long term low dose aspirin
management of patients with mechanical valves
low failure rate
increased risk of thrombosis - long term warfarin and low dose aspirin
target INR - aortic (3), mitral (3.5)
significance of pulmonary artery occlusion pressure monitoring
indirect measure of left atrial pressure and filling pressure of left heart
normal - 8-12mmHg
features of pulmonary embolism
chest pain
typically pleuritic
dyspnoea
haemoptysis
tachycardia
tachypnoea
respiratory examination
The relative frequency of common clinical signs is shown below:
Tachypnea (respiratory rate >16/min) - 96%
Crackles - 58%
Tachycardia (heart rate >100/min) - 44%
Fever (temperature >37.8°C) - 43%
what is the PERC
used to exclude PE in patients with low pre-test probability
age >50
HR >100
O2 <94
prev DVT/PE
recent surgery <4w
haemoptysis
unilateral leg swelling
oestrogen use
if all absent, PE probability <2%
when to use 2 level PE wells score (and features)
when PE is suspected
Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
An alternative diagnosis is less likely than PE 3
Heart rate > 100 beats per minute 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1
Malignancy (on treatment, treated in the last 6 months, or palliative)
how to interpret a wells score
if PE likely (>4 pt) - CTPA, therapeutic anticoagulation until scan performed
if CTPA negative consider proximal leg vein USS
if PE unlikely - d dimer, if + do CTPA, if - consider alternative diagnosis
when to use CTPA vs VQ scan
CTPA preferred
VQ if renal impairment as no need for contrast
investigation findings in PE
d dimer - high sensitivity, low specificity - +++
ECG - S1Q3T3, RBBB, sinus tachycardia
CXR - usually normal, may have wedge-shaped opacification
CTPA - peripheral emboli may be missed
VQ scan - mismatch
drugs used in managing VTE
DOAC - apixaban, rivaroxaban once diagnosis suspected, continue if dx confirmed
if DOAC is C/I
LMWH then dabigatran/edoxaban
severe renal impairment - LMWH, unfractionated heparin
if haemodynamically unstable - thrombolysis
duration of anticoagulation therapy in VTE
ALL 3m
if provoked - stop after 3m
if cancer - stop after 3-6m
if unprovoked - 6m
meaning of pulsus paradoxus + causes
greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration
severe asthma, cardiac tamponade
meaning of slow rising pulse + causes
Slow-rising/plateau
aortic stenosis
meaning of collapsing pulse + causes
aortic regurgitation
patent ductus arteriosus
hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)
meaning of pulsus alternans + causes
regular alternation of the force of the arterial pulse
severe LVF
meaning of bisferiens pulse + causes
‘double pulse’ - two systolic peaks
mixed aortic valve disease
meaning of jerky pulse + causes
hypertrophic obstructive cardiomyopathy*
causes and diagnosis of rheumatic fever
develops following an immunological reaction to a recent (2-4 weeks ago) Streptococcus pyogenes infection
Diagnosis is based on evidence of recent streptococcal infection accompanied by:
2 major criteria
1 major with 2 minor criteria
criteria for diagnosing rheumatic fever
Evidence of recent streptococcal infection
raised or rising streptococci antibodies,
positive throat swab
positive rapid group A streptococcal antigen test
major criteria
erythema marginatum
Sydenham’s chorea
polyarthritis
carditis and valvulitis (eg, pancarditis)
subcut nodules
Minor criteria
raised ESR or CRP
pyrexia
arthralgia (not if arthritis a major criteria)
prolonged PR interval
management of rheumatic fever
antibiotics: oral penicillin V
anti-inflammatories: NSAIDs are first-line
treatment of any complications that develop e.g. heart failure
adverse effects of statins
myopathy
liver impairment - check LFT at baseline, 3m, 12m
contraindications to statin therapy
macrolides - stop statin until pt completes course of ABx
pregnancy
indications for statin therapy
all pt with established CVS risk
anyone with 10 year CVS risk >10%
T1DM pt diagnosed >10years ago or >40y or established nephropathy
doses of statins for prevention of CVS disease
atorvastatin 20mg - primary prevention
atorvastatin 80mg for secondary prevention
what are the characteristics and definition of an SVT
sudden onset narrow complex tachycardia
usually AVNRT, AVRT, junctional tachy
management and prevention of supraventricular tachycardias
vagal manouvres - valsalva, carotid sinus massage
IV adenosine - rapid bolus 6mg -> 12mg -> 18mg
(C/I in asthmatics)
electrical cardioversion
prevention - beta-blockers
radiofrequency ablation
definition and main causes of syncope
a transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery
reflex
orthostatic
cardiac
causes of reflex syncope
vasovagal: triggered by emotion, pain or stress. Often referred to as ‘fainting’
situational: cough, micturition, gastrointestinal
carotid sinus syncope
most common in all age groups
causes of orthostatic syncope
primary autonomic failure: Parkinson’s disease, Lewy body dementia
secondary autonomic failure: e.g. Diabetic neuropathy, amyloidosis, uraemia
drug-induced: diuretics, alcohol, vasodilators
volume depletion: haemorrhage, diarrhoea
causes of cardiac syncope
arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular)
structural: valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy
others: pulmonary embolism
how to investigate a patietn with syncope
cardiovascular examination
postural blood pressure readings: a symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg is considered diagnostic
ECG for all patients
other tests depend on clinical features
patients with typical features, no postural drop and a normal ECG do not require further investigations
features and management of syndrome X
angina-like chest pain on exertion
ST depression on exercise stress test
but normal coronary arteries on angiography
nitrates
definition and features of takayasu’s arteritis
large vessel vasculitis causing occlusion of aorta, causing absent limb pulse
most common in younger females and asians
features
systemic features of a vasculitis e.g. malaise, headache
unequal blood pressure in the upper limbs
carotid bruit and tenderness
absent or weak peripheral pulses
upper and lower limb claudication on exertion
aortic regurgitation (around 20%)
investigations and management of takayasu’s arteritis
Investigations
vascular imaging of the arterial tree is required to make a diagnosis of Takayasu’s arteritis
either magnetic resonance angiography (MRA) or CT angiography (CTA)
Management
steroids
definition and features of takotsubo cardiomyopathy
non-ischaemic cardiomyopathy associated with a transient, apical ballooning of the myocardium, may be triggered by stress
chest pain
features of heart failure
ECG: ST-elevation
normal coronary angiogram
supportive treatment
moa and adverse effecs of thiazide diuretics
inhibit sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter - causes K+ loss
prev used in HTN but now replaced by thiazide- like diuretics e.g., indapamide
S/E
dehydration
postural hypotension
hypokalaemia
hyponatraemia
hypercalcaemia
action of thrombolytic drugs
thrombolytic drugs activate plasminogen to form plasmin - degrades fibrin, breaks down thrombi - used in STEMI, acute ischaemic stroke, PE
examples - alteplase, tenecteplase, streptoinase
contraindications to thrombolysis
active internal bleeding
recent haemorrhage, trauma or surgery (including dental extraction)
coagulation and bleeding disorders
intracranial neoplasm
stroke < 3 months
aortic dissection
recent head injury
severe hypertension
definition and causes of torsades de pointes
form of polymorphic ventricular tachycardia associated with a long QT interval - deteriorates into VF, leads to sudden death
causes
congenital
antiarhythmics
tricyclic antidepressants
antipsychotics
chloroquine
terfenadine
erythromycin
management of torsades de pointes
IV magnesium sulphate
signs of tricuspid regurgitation
pan-systolic murmur
prominent/giant V waves in JVP
pulsatile hepatomegaly
left parasternal heave
causes of tricuspid regurgitation
right ventricular infarction
pulmonary hypertension e.g. COPD
rheumatic heart disease
infective endocarditis (especially intravenous drug users)
Ebstein’s anomaly
carcinoid syndrome
steps of the valsalva manouvre
- Increased intrathoracic pressure
- Resultant increase in venous and right atrial pressure reduces venous return
- The reduced preload leads to a fall in the cardiac output (Frank-Starling mechanism)
- When the pressure is released there is a further slight fall in cardiac output due to increased aortic volume
- Return of normal cardiac output
causes of ventricular septal defect
most common cause of congenital heart disease - close spontaneously in around 50% of cases.
congenital VSDs are often association with chromosomal disorders
(Down’s syndrome, Edward’s syndrome, Patau syndrome, cri-du-chat syndrome)
congenital infections
acquired causes - post-myocardial infarction
management of ventricular septal defects
small, asymptomatic VSF - close spontaneously, need monitoring
moderate - large - cause HF in few months - give medication of HF (diuretics), surgical closure of defect
may cause eisenmenger’s, RHF, pulmonary HTN
types of ventricular tachycardia
monomorphic VT: most commonly caused by myocardial infarction
polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval
management of ventricular tachycardia
f the patient has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure) then immediate cardioversion is indicated
amiodarone: ideally administered through a central line
lidocaine: use with caution in severe left ventricular impairment
procainamide
Verapamil should NOT be used in VT
moa of warfarin
inhibits epoxide reductase preventing the reduction of vitamin K to its active hydroquinone form
this in turn acts as a cofactor in the carboxylation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.
indications for warfarin
mechanical heart valves - INR 3 for aortic, 3.5 for mitral
used second line to DOAC - VTE INR 2.5, recurrent VTE 3.5, AF INR 2.5
factors potentiating warfarin
liver disease
P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin
cranberry juice
drugs which displace warfarin from plasma albumin, e.g. NSAIDs
inhibit platelet function: NSAIDs
p450 inducers
antiepileptics: phenytoin, carbamazepine
barbiturates: phenobarbitone
rifampicin
St John’s Wort
chronic alcohol intake
griseofulvin
smoking (affects CYP1A2, reason why smokers require more aminophylline)
p450 inhibitors
antibiotics: ciprofloxacin, clarithromycine/erythromycin
isoniazid
cimetidine,omeprazole
amiodarone
allopurinol
imidazoles: ketoconazole, fluconazole
SSRIs: fluoxetine, sertraline
ritonavir
sodium valproate
acute alcohol intake
quinupristin
management guidelines for high INR
major bleeding - stop warfarin, IV VK 5mg, prothrombin complex concentrate
INR >8 + minor bleeding - stop warfarin, IV VK 1-3mg, restart warfarin when INR <5
INR >8 no bleeding - stop warfarin, vitamin K 1-5mg, restart when INR <5
INR 5-8 minor bleeding - stop warfarin, IV VK 1-3mg, restart when INR <5
INR 5-8 no bleeding - withhold 1-2 doses, reduce subsequent maintenance dose
features of wolff-parkinson white
due to a congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT)
the accessory pathway does not slow conduction so AF can degenerate rapidly to VF
ECG features of WPW
short PR interval
wide QRS complexes with a slurred upstroke - ‘delta wave’
left axis deviation if right-sided accessory pathway
right axis deviation if left-sided accessory pathway
treatment of wolff parkinson white
definitive treatment: radiofrequency ablation of the accessory pathway
medical therapy: sotalol, amiodarone, flecainide
