Cardiology Flashcards

(119 cards)

1
Q

Causes of Reversed splitting of second heart sound

A

1- Aortic stenosis
2- LBBB
3- HOCM

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2
Q

Causes of Fixed splitting of second heart sound

A

1-ASD
2-VSD

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3
Q

Cerebral infarct following treatment of a DVT

A

Patent Foramen Ovale

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4
Q

Pulse pressure

A

Decreased aortic compliance with increasing age leads to increased pulse pressure.

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5
Q

Long QT syndrome Type 1

A

KCNQ1 gene isolated to chromosome 11.
KCNQ1 codes for voltage gated potassium channel. This is a slow delayed rectifier potassium channel mutation.

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6
Q

Long QT syndrome

A

1- Romano ward syndrome
LQT1
LQT2
LQT3
2- Jervell and Lange Nielson syndrome
3- Anderson and Tawil syndrome
4- Timothy syndrome
5- Acquired causes
DRUGS ASH-FECT
Electrolyte abnormalities HypoKMC

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7
Q

Prolonged QT

A

QTc >440ms in men and >460ms in women

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8
Q

Mitral Stenosis

A

-Diastolic Murmur
-Apical Thrill
-Right ventricular heave/ Loud P2
-Pulm Regurg ( Graham steel Murmur)
-Low pulse pressure
-Soft S1

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9
Q

Mitral Regurgitation

A

-pansystolic murmur
- Small volume pulse
-Presence of S3
- Displaced and hyperdynamic apex

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10
Q

Aortic Regurgitation

A

-Quincke sign
-Corrigans pulse
- Corrigans sign
-De Musset sign
- Duroziez sign
- Traube sign
- Austin Flint murmur
- Aurgyl Robertson pupils
- Muller sign

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11
Q

Aortic Stenosis

A
  • Slow-rising pulse with narrow pulse pressure
  • S4
  • Presence of precordial thrill
  • Absent A2
  • Paradoxically split A2
  • Symptoms of syncope or left ventricular failure
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12
Q

HCM

A
  • Jerky pulse with large tidal wave.
  • Large A waves in JVP.
  • Double apical impulse.
  • Left sternal edge systolic thrill with harsh ejection systolic murmur radiating to the axilla.
  • often accompanied by MR.
  • often paradoxical splitting of S2.
  • The ejection systolic murmur increases with the Valsalva maneuver and decreases with squatting.
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13
Q

Classification of Haemorrhage

A

Classification of haemorrhage:

Parameter I II III IV
Blood loss (ml) <750 750-1500 1500-2000 >2000
Blood loss (%) <15% 15-30% 30-40% >40%
Pulse rate (beats/min) <100 >100 >120 >140
Blood pressure Normal Normal/Decreased Decreased Decreased
Respiratory rate (breaths/min) 14-20 20-30 30-40 >35
Urine output (ml/hour) >30 20-30 5-15 Negligible
CNS symptoms Normal Anxious Confused Lethargic

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14
Q

Arrhythmogenic right ventricular cardiomyopathy

A
  • autosomal dominant pattern
    -The right ventricular myocardium is replaced by fatty and fibrofatty tissue
    -ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV. This is best described as a terminal notch in the QRS complex. Echo shows an enlarged, hypokinetic right ventricle with a thin free wall.
    Rx is Sotalol, Catheter ablation, and ICD.
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15
Q

Naxos Disease

A

-an autosomal recessive variant of ARVC
- a triad of ARVC, palmoplantar keratosis, and woolly hair

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16
Q

Coarctation of aorta

A

-Difference in blood pressures between the right and left arms.
-Radiofemoral delay
-Systolic murmur and thrill
-Headache and nose bleeds occur due to hypertension.
-Chest radiograph demonstrates evidence of rib notching and may demonstrate an indentation of the aortic shadow at the site of the coarctation.
-Rx is balloon angioplasty and stenting.

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17
Q

Macrophages

A

Macrophages are involved in coronary artery plaques

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18
Q

Dapagliflozin

A

Dapagliflozin is a sodium-glucose co-transporter 2 (SGLT2) inhibitor shown to reduce the risk of worsening heart failure and cardiovascular death in patients with heart failure with preserved and mildly reduced ejection fraction. It is an appropriate addition to the current regimen for symptomatic relief and long-term cardiovascular benefit in this patient population.

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19
Q

Antibiotic prophylaxis against Infective Endocarditis

A

According to NICE guidelines, antibiotic Prophylaxis against infective endocarditis (CG64) is not recommended in common cardiac valve abnormalities.

Prophylaxis is only recommended in those patients who are at highest risk of adverse outcomes on the development of endocarditis. These patient groups include:

acquired valvular heart disease with stenosis or regurgitation

hypertrophic cardiomyopathy
previous infective endocarditis

structural congenital heart disease, including surgically corrected or palliated structural conditions, but excluding isolated atrial septal defect, fully repaired ventricular septal defect or fully repaired patent ductus arteriosus, and closure devices that are judged to be endothelialised
valve replacement.

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20
Q

Constrictive pericarditis

A

Constrictive pericarditis typically impedes late diastolic ventricular filling, which produces an elevated jugular venous pressure (JVP), with prominent x and y descent.

Other signs include:
- Oedema
- Ascites
- Hepatomegaly
- Orthopnoea
- Dyspnoea.

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21
Q

ACS ( Poor prognostic Factors)

A

ACS- poor Prognostic factors

  • age
  • development (or history) of heart failure
  • peripheral vascular disease
  • reduced systolic blood pressure
  • Killip class*
  • initial serum creatinine concentration
  • elevated initial cardiac markers
  • cardiac arrest on admission
  • ST segment deviation
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22
Q

Heart Failure Rx

  • AB
    -AS
    -ISD
A

First-line therapy

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

Second-line therapy

The standard second-line treatment is an aldosterone antagonist
these are sometimes referred to as mineralocorticoid receptor antagonists. 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

There is an increasing role for SGLT-2 inhibitors in the management of heart failure with a reduced ejection fraction
these drugs reduce glucose reabsorption and increase urinary glucose excretion
examples include canagliflozin, dapagliflozin and empagliflozin
the evidence base shows SGLT-2 inhibitors reduced hospitalisation secondary to heart failure and cardiovascular death
international guidelines widely recommend their usage. In terms of NICE, a technology appraisal from 2021 support the use of dapagliflozin as an add-on to optimised standard care

Third-line therapy

Third-line treatment should be initiated by a specialist. Options include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy
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

Other treatments
offer annual influenza vaccine
offer one-off pneumococcal vaccine

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23
Q

Naftidrofuryl

A

Naftidrofuryl is a 5-HT2 receptor antagonist which can be used for peripheral vascular disease

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24
Q

Aortic Regurgitation

A
  • 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
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25
Selenium
Selenium deficiency is known to cause Keshan disease, a type of dilated cardiomyopathy.
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Dilated 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 + these causes may also lead to restrictive cardiomyopathy - nutritional e.g. wet beriberi (thiamine deficiency
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Prominent V waves
Prominent V waves on JVP → tricuspid regurgitation
28
Atrial Fibrillation
Onset < 48 hours If the atrial fibrillation (AF) is definitely of less than 48 hours onset patients should be heparinised. Patients who have risk factors for ischaemic stroke should be put on lifelong oral anticoagulation. Otherwise, patients may be cardioverted using either: electrical - 'DC cardioversion' pharmacology - amiodarone if structural heart disease, flecainide or amiodarone in those without structural heart disease Following electrical cardioversion if AF is confirmed as being less than 48 hours duration then further anticoagulation is unnecessary Onset > 48 hours If the patient has been in AF for more than 48 hours then anticoagulation should be given for at least 3 weeks prior to cardioversion. An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded patients may be heparinised and cardioverted immediately. NICE recommend electrical cardioversion in this scenario, rather than pharmacological. If there is a high risk of cardioversion failure (e.g. Previous failure or AF recurrence) then it is recommend to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this time decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence
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Complete heart block following a MI?
- right coronary artery lesion
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Complete Heart Block
Features - syncope - heart failure - regular bradycardia (30-50 bpm) - wide pulse pressure - JVP: cannon waves in neck - variable intensity of S1 Types of heart block - First degree heart block PR interval > 0.2 seconds - Second degree heart block type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex - Third degree (complete) heart block there is no association between the P waves and QRS complexes
31
Arrhythmogenic right ventricular cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy is characterised by right ventricular myocardium replaced by fatty and fibrofatty tissue. Investigation ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex echo changes are often subtle in the early stages but may show an enlarged, hypokinetic right ventricle with a thin free wall magnetic resonance imaging is useful to show fibrofatty tissue Management drugs: sotalol is the most widely used antiarrhythmic Catheter ablation to prevent ventricular tachycardia implantable cardioverter-defibrillator Naxos disease an autosomal recessive variant of ARVC a triad of ARVC, palmoplantar keratosis, and woolly hair.
32
CPVT
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a form of inherited cardiac disease associated with sudden cardiac death. It is inherited in an autosomal dominant fashion and has a prevalence of around 1:10,000. Pathophysiology the most common cause is a defect in the ryanodine receptor (RYR2) which is found in the myocardial sarcoplasmic reticulum Features exercise or emotion induced polymorphic ventricular tachycardia resulting in syncope sudden cardiac death symptoms generally develop before the age of 20 years Management - beta-blockers - implantable cardioverter-defibrillator
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Mechanical Valve
The most common type now implanted is the bileaflet valve. Ball-and-cage valves are rarely used nowadays Mechanical valves have a low failure rate Major disadvantage is the increased risk of thrombosis meaning long-term anticoagulation is needed. Warfarin is still used in preference to DOACs for patients with mechanical heart valves Following the 2017 European Society of Cardiology guidelines, aspirin is only normally given in addition if there is an additional indication, e.g. ischaemic heart disease. Target INR aortic: 3.0 mitral: 3.5
35
BNP
B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain. Very high levels are associated with a poor prognosis. BNP NTproBNP High levels > 400 pg/ml (116 pmol/litre) > 2000 pg/ml (236 pmol/litre) Raised levels 100-400 pg/ml (29-116 pmol/litre) 400-2000 pg/ml (47-236 pmol/litre) Normal levels < 100 pg/ml (29 pmol/litre) < 400 pg/m
36
Increase BNP Causes
Left ventricular hypertrophy Ischaemia Tachycardia Right ventricular overload Hypoxaemia (including pulmonary embolism) GFR < 60 ml/min Sepsis COPD Diabetes Age > 70 Liver cirrhosis
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Decrease BNP causes
Obesity Diuretics ACE inhibitors Beta-blockers Angiotensin 2 receptor blockers Aldosterone antagonists
38
Jugular venous pulse
a' wave = atrial contraction large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension absent if in atrial fibrillation Cannon 'a' waves caused by atrial contractions against a closed tricuspid valve are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing 'c' wave closure of tricuspid valve not normally visible 'v' wave due to passive filling of blood into the atrium against a closed tricuspid valve giant v waves in tricuspid regurgitation 'x' descent = fall in atrial pressure during ventricular systole 'y' descent = opening of tricuspid valve
39
SVT
Acute management - vagal manoeuvres: - Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe carotid sinus massage - intravenous adenosine rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg contraindicated in asthmatics - verapamil is a preferable option electrical cardioversion - Prevention of episodes beta-blockers radio-frequency ablation
40
Takotsubo Cardiomyopathy
Takotsubo cardiomyopathy also known as 'Broken heart syndrome' and 'Takotsubo apical ballooning syndrome' describes a cardiomyopathy induced by severe stressful triggers (e.g. emotional upset). It is commoner in women. In this scenario, we assume that the patient is in bereavement which precipitated the stress cardiomyopathy. Takotsubo is a Japanese word that describes an octopus trap; this is used to describe the appearance of the heart on left ventriculogram, CMR or echocardiogram. This apical ballooning appearance occurs due to severe hypokinesis of the mid and apical segments with preservation of activity of the basal segments. In simple terms, the bottom of the heart (the apex) does not contract and therefore appears to balloon out. However, the area closer to the top (the base) continues to contract (creating the neck of the octopus trap).
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Reversible causes of cardiac arrest
5H - Hypoxia - Hypovolaemia -Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders - Hypothermia - Thrombosis (coronary or pulmonary) - Tension pneumothorax - Tamponade - cardiac - Toxins
44
VSD ( Ventricular septal Defect)
Ventricular septal defects (VSD) are the most common cause of congenital heart disease. They close spontaneously in around 50% of cases. Aetiology - 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 VSDs may be detected in utero during the routine 20 week scan. Post-natal presentations include: - Failure to thrive - Features of heart failure - hepatomegaly - Tachypnoea - Tachycardia - Pallor Classically a pan-systolic murmur which is louder in smaller defects Management is clearly highly specialised small VSDs that are asymptomatic often close spontaneously and simply require monitoring moderate to large VSDs usually result in a degree of heart failure in the first few months nutritional support medication for heart failure e.g. diuretics surgical closure of the defect Complications - Aortic regurgitation Aortic regurgitation is due to a poorly supported right coronary cusp resulting in cusp prolapse infective endocarditis - Eisenmenger's complex due to prolonged pulmonary hypertension from the left-to-right shunt results in right ventricular hypertrophy and increased right ventricular pressure. This eventually exceeds the left ventricular pressure resulting in a reversal of blood flow this in turn results in cyanosis and clubbing Eisenmenger's complex is an indication for a heart-lung transplant - Right heart failure - Pulmonary hypertension Pregnancy is contraindicated in women with pulmonary hypertension as it carries a 30-50% risk of mortality
45
Culture negative Endocarditis
Q fever is caused by Coxiella burnetii, a rickettsia. The source of infection is typically an abattoir, cattle/sheep, or it may be inhaled from infected dust. Features Typically prodrome: - fever, malaise - causes pyrexia of unknown origin - Transaminitis. - atypical pneumonia - endocarditis (culture-negative) Management - Doxycycline
46
Infective Endocarditis Treatment
>>Initial blind therapy 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 >>Native valve endocarditis caused by staphylococci Flucloxacillin if penicillin allergic or MRSA vancomycin + rifampicin >>Prosthetic valve endocarditis caused by staphylococci Flucloxacillin + rifampicin + low-dose gentamicin If penicillin allergic or MRSA vancomycin + rifampicin + low-dose gentamicin >>Endocarditis caused by fully-sensitive streptococci (e.g. viridans) Benzylpenicillin If penicillin allergic vancomycin + low-dose gentamicin >>Endocarditis caused by less sensitive streptococci Benzylpenicillin + low-dose gentamicin If penicillin allergic vancomycin + low-dose gentamicin
47
Dabigatran antidote
Idarucizumab ( praxbind) is a recently developed monoclonal antibody fragment which binds dabigatran with an affinity that is 350 times as high as with thrombin. Consequently, idarucizumab binds free and thrombin-bound dabigatran and rapidly neutralises its activity
48
DVLA: cardiovascular disorders
>>Angioplasty (elective) - 1 week off driving >>CABG - 4 weeks off driving >>acute coronary syndrome- 4 weeks off driving >>1 week if successfully treated by angioplasty >>Angina - driving must cease if symptoms occur at rest/at the wheel >>Pacemaker insertion - 1 week off driving >>Implantable cardioverter-defibrillator (ICD) if implanted for sustained ventricular arrhythmia, cease driving for 6 months if implanted prophylactically then cease driving for 1 month. Having an ICD results in a permanent bar for Group 2 drivers >>successful catheter ablation for an arrhythmia- 2 days off driving aortic aneurysm of 6cm or more - notify DVLA. Licensing will be permitted subject to annual review. an aortic diameter of 6.5 cm or more disqualifies patients from driving. >>heart transplant: do not drive for 6 weeks, no need to notify DVLA
49
Stable Angina Ix
1st line: CT coronary angiography 2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia) 3rd line: invasive coronary angiography
50
Non invasive Functional imaging
Examples of non-invasive functional imaging: 1- myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or 2- stress echocardiography or first-pass contrast-enhanced magnetic 3- resonance (MR) perfusion or MR imaging for stress-induced wall motion abnormalities
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Mitral Valve Prolapse
Associations - Congenital heart disease: PDA, ASD - Cardiomyopathy - Turner's syndrome - Marfan's syndrome, Fragile X - Osteogenesis imperfecta - Pseudoxanthoma elasticum - Wolff-Parkinson White syndrome - long-QT syndrome - Ehlers-Danlos Syndrome - Polycystic kidney disease
53
Flecainide
Flecainide is a Vaughan Williams class 1c antiarrhythmic. It slows conduction of the action potential by acting as a potent sodium channel blocker (specifically the Nav1.5 sodium channels). This may be reflected by widening of the QRS complex and prolongation of the PR interval.
54
Familial Hypercholesterolemia ( Simon Broome Criteria)
In adults total cholesterol (TC) > 7.5 mmol/l and LDL-C > 4.9 mmol/l
55
Statins in Pregnancy
Statins are contraindicated during pregnancy as they cross the placental barrier and may cause foetal harm. There is evidence that statins can interfere with cholesterol-dependent embryonic development and may be teratogenic. Guidelines recommend discontinuing statins at least 3 months before planned conception and throughout pregnancy.
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Acyanotic Congenital Heart Diseases
-Ventricular septal defects (VSD) - most common, accounts for 30% - Atrial septal defect (ASD) - Patent ductus arteriosus (PDA) - Coarctation of the aorta - Aortic valve stenosis
57
Cyanotic Congenital Heart Diseases
3T - Tetralogy of Fallot - transposition of the great arteries (TGA) - tricuspid atresia Fallot's is more common than TGA but TGA is most common at birth.
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Pre- Existing Hypertension
A history of hypertension before pregnancy or an elevated blood pressure > 140/90 mmHg before 20 weeks gestation
59
Pregnancy induced HTN / Gestational HTN
Hypertension (as defined above) occurring in the second half of pregnancy (i.e. after 20 weeks)
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Pre-Eclampsia
Pregnancy-induced hypertension in association with proteinuria (> 0.3g / 24 hours)
61
Aortic Dissection
Aortic dissection type A - ascending aorta - control BP (IV labetalol) + surgery type B - descending aorta - control BP(IV labetalol)
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IE
Antibiotic prohylaxis to prevent infective endocarditis is not routinely recommended in the UK for dental and other procedures
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DVLA in LVF
An LVEF of < 40% bars him from driving a lorry, even if he becomes asymptomatic with treatment
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Pulses
Pulsus paradoxus greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration severe asthma, cardiac tamponade Slow-rising/plateau aortic stenosis Collapsing aortic regurgitation patent ductus arteriosus hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy) Pulsus alternans regular alternation of the force of the arterial pulse severe LVF Bisferiens pulse 'double pulse' - two systolic peaks mixed aortic valve disease 'Jerky' pulse hypertrophic obstructive cardiomyopathy* *HOCM may occasionally be associated with a bisferiens pulse
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HTN
For patients of black African or African-Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor
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Hypertrophic obstructive cardiomyopathy (HOCM)
Hypertrophic obstructive cardiomyopathy (HOCM) is an autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins. The estimated prevalence is 1 in 500. Management Amiodarone Beta-blockers or verapamil for symptoms Cardioverter defibrillator Dual chamber pacemaker Endocarditis prophylaxis* Drugs to avoid nitrates ACE-inhibitors inotropes
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Amiodarone
All antiarrhythmic drugs have the potential to cause arrhythmias. Coexistent hypokalaemia significantly increases this risk.
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Amiodarone
Amiodarone is a class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias. The main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)
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Monitoring of patients taking amiodarone
Monitoring of patients taking amiodarone TFT, LFT, U&E, CXR prior to treatment TFT, LFT every 6 months
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Adverse effects of Amiodarone use
- thyroid dysfunction: both hypothyroidism and hyperthyroidism - corneal deposits - pulmonary fibrosis/pneumonitis - Liver fibrosis/hepatitis - peripheral neuropathy, myopathy - photosensitivity - 'slate-grey' appearance - thrombophlebitis and injection site reactions - bradycardia - lengths QT interval
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Pulmonary Arterial HTN
- If there is a positive response to acute vasodilator testing (a minority of patients) oral calcium channel blockers If there is a negative response to acute vasodilator testing (the vast majority of patients) - prostacyclin analogues: treprostinil, iloprost - endothelin receptor antagonists non-selective: bosentan - selective antagonist of endothelin receptor A: ambrisentan - phosphodiesterase inhibitors: sildenafil
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Pulmonary arterial hypertension (PAH)
Pulmonary arterial hypertension (PAH) may be defined as a resting mean pulmonary artery pressure of >= 20 mmHg. Endothelin is thought to play a key role in the pathogenesis of PAH. It is more common in females and typically presents between the ages of 30-50 years
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Clinical signs of Pulmonary HTN
- Right ventricular heave - Loud P2 - Raised JVP with prominent a waves - Tricuspid regurgitation
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QRISK2 for type 1 Diabetics
NICE specifically state that we should not use QRISK2 for type 1 diabetics. Instead, the following criteria are used: older than 40 years, or have had diabetes for more than 10 years or have established nephropathy or have other CVD risk factors
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Hypertension in Pregnancy
Hypertension in pregnancy in usually defined as: systolic > 140 mmHg or diastolic > 90 mmHg or an increase above booking readings of > 30 mmHg systolic or > 15 mmHg diastolic
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Ticagrelor
Dyspnoea is a common side effect of ticagrelor and is estimated to occur in up to 15% of patients started on this medication. It is hypothesised that the sensation of dyspnoea in ticagrelor-treated patients is triggered by adenosine, because ticagrelor inhibits its clearance (by inhibiting the enzyme adenosine deaminase), thereby increasing its concentration in the circulation.
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Complications of VSD
- Aortic regurgitation - Infective endocarditis - Eisenmenger's complex d Eisenmenger's complex is an indication for a heart-lung transplant - Right heart failure - pulmonary hypertension Pregnancy is contraindicated in women with pulmonary hypertension as it carries a 30-50% risk of mortality
78
VSDs
Ventricular septal defects (VSD) are the most common cause of congenital heart disease. They close spontaneously in around 50% of cases. Aetiology Congenital VSDs are often association with chromosomal disorders - Down syndrome - Edward's syndrome - Patau syndrome - cri-du-chat syndrome - congenital infections acquired causes - post-myocardial infarction
79
Severe Pre-eclampsia
Severe pre-eclampsia - restrict fluids Important for meLess important Restrictions of fluids to 80 mL/hr i
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Primary prevention of CVD
In the primary prevention of CVD using statins aim for a reduction in non-HDL cholesterol of > 40%
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Murmurs
RILE Right-sided murmur → heard best on Inspiration Left-sided murmur → heard best on Expiration
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Recurrent DVTs
Patients with recurrent venous thromboembolic disease may be considered for an inferior vena cava filter.
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Warfarin INR Targets
Target INR aortic: 3.0 mitral: 3.5
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Flecainide
Flecainide is a Vaughan Williams class 1c antiarrhythmic. It slows conduction of the action potential by acting as a potent sodium channel blocker (specifically the Nav1.5 sodium channels). This may be reflected by widening of the QRS complex and prolongation of the PR interval.
87
Flecainide
Adverse effects negatively inotropic bradycardia proarrhythmic oral paraesthesia visual disturbances
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Causes of Axis Deviation
Causes of left axis deviation (LAD) 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 (RAD) 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
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Ivabradine
Ivabradine use may be associated with visual disturbances including phosphenes and green luminescence
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Wide pulse pressure
In older adults, the main factor that accounts for a large pulse pressure is reduced aortic compliance
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Idiopathic Intracranial HTN
Obese, young female with headaches / blurred vision think idiopathic intracranial hypertension
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Idiopathic Intracranial HTN
- Weight Loss - Carbonic anhydrase inhibitors e.g. acetazolamide - topiramate, is also used, and has the added benefit of causing weight loss in most patients - Repeated lumbar puncture may be used as a temporary measure but is not suitable for longer-term management - Surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure
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Infective Endocarditis
Poor prognostic factors Staphylococcus aureus infection (see below) prosthetic valve (especially 'early', acquired during surgery) culture negative endocarditis low complement levels Mortality according to organism staphylococci - 30% bowel organisms - 15% streptococci - 5%
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IE
Infective endocarditis - streptococcal infection carries a good prognosis
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bendroflumethiazide
bendroflumethiazide acts at the proximal part of the distal convoluted tubules
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MAO inhibitors ( Phenelzine)
Foods to avoid - tyramine-containing foods e.g. cheese, pickled herring, Bovril, Oxo, Marmite, broad beans
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JVP: Cannon waves
JVP: cannon waves Caused by the right atrium contracting against a closed tricuspid valve. May be subdivided into regular or intermittent - Regular cannon waves ventricular tachycardia (with 1:1 ventricular-atrial conduction) Atrioventricular nodal re-entry tachycardia (AVNRT) - Irregular cannon waves Complete heart block
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Severe Aortic Stenosis
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
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ASDs
Atrial septal defects (ASDs) are the most likely congenital heart defect to be found in adulthood. They carry a significant mortality, with 50% of patients being dead at 50 years. Two types of ASDs are recognised, ostium secundum and ostium primum. Ostium secundum are the most common 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% of ASDs) associated with Holt-Oram syndrome (tri-phalangeal thumbs) ECG: RBBB with RAD Ostium primum present earlier than ostium secundum defects associated with abnormal AV valves ECG: RBBB with LAD, prolonged PR interval
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Long QT syndrome
Long QT syndrome - usually due to loss-of-function/blockage of K+ channels
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Takayasu’s arteritis
Takayasu's arteritis Takayasu's arteritis is a large vessel vasculitis. It typically causes occlusion of the aorta and questions commonly refer to an absent limb pulse. It is more common in younger females (e.g. 10-40 years) and Asian people. 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%) Associations renal artery stenosis 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
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Causes of ST depression
Causes of ST depression - secondary to abnormal QRS (LVH, LBBB, RBBB) - ischaemia - digoxin - hypokalaemia - syndrome X
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Mitral Stenosis
In mitral stenosis, an opening snap indicates the leaflets still have some mobility
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Dentistry in warfarinised patients
Dentistry in warfarinised patients - check INR 72 hours before procedure, proceed if INR < 4.0
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Chronic Heart Failure
NICE guidelines recommend the introduction of an ACE inhibitor prior to a beta-blocker in patients with chronic heart failure
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Dipyridamole
Mechanism of action inhibits phosphodiesterase, elevating platelet cAMP levels which in turn reduce intracellular calcium levels other actions include reducing cellular uptake of adenosine and inhibition of thromboxane synthase
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Aortic Dilatation
An increased risk of aortic dilatation and dissection is the most serious long-term health problem for women with Turner's syndrome
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Pulmonary arterial hypertension
Pulmonary arterial hypertension (PAH) may be defined as a resting mean pulmonary artery pressure of >= 20 mmHg. Endothelin is thought to play a key role in the pathogenesis of PAH. It is more common in females and typically presents between the ages of 30-50 years.
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Pulmonary arterial hypertension
If there is a positive response to acute vasodilator testing (a minority of patients) oral calcium channel blockers If there is a negative response to acute vasodilator testing (the vast majority of patients) - prostacyclin analogues: treprostinil, iloprost - endothelin receptor antagonists non-selective: bosentan selective antagonist of endothelin receptor A: ambrisentan - phosphodiesterase inhibitors: sildenafil Patients with progressive symptoms should be considered for a heart-lung transplant.
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Pulses
Pulsus paradoxus greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration severe asthma, cardiac tamponade Slow-rising/plateau aortic stenosis Collapsing aortic regurgitation patent ductus arteriosus hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy) Pulsus alternans regular alternation of the force of the arterial pulse severe LVF Bisferiens pulse 'double pulse' - two systolic peaks mixed aortic valve disease 'Jerky' pulse hypertrophic obstructive cardiomyopathy* *HOCM may occasionally be associated with a bisferiens pulse
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Pulsus Alternans
Pulsus alternans - seen in left ventricular failure
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S2
Causes of a loud S2 hypertension: systemic (loud A2) or pulmonary (loud P2) hyperdynamic states atrial septal defect without pulmonary hypertension Causes of a 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 Causes of a reversed (paradoxical) split S2 (P2 occurs before A2) LBBB severe aortic stenosis right ventricular pacing WPW type B (causes early P2) patent ductus arteriosus
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Aspirin
Aspirin is a non-reversible COX 1 and 2 inhibitor. -Aspirin is a non-reversible inhibitor of COX 1 and COX 2. It inhibits the conversion of arachidonic acid to prostaglandin, prostacyclin, and thromboxane. Thromboxane A2 promotes platelet aggregation and vasoconstriction. High-dose aspirin is given acutely in acute coronary syndrome to prevent enlargement of the coronary thrombus.
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Hyperuricaemia
Hyperuricaemia may be associated with both hyperlipidaemia and hypertension. It may also be seen in conjunction with the metabolic syndrome
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Mechanism of Action of Warfarin
Mechanism of action 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.
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Second heart sound (S2)
Second heart sound (S2) loud: hypertension soft: AS fixed split: ASD reversed split: LBBB
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