Cardiology Flashcards

(123 cards)

1
Q

What is S4 heart sound and which part of the ECG does this sound coincide with?

A

S4 heart sound is caused by atrial contraction against a stiff ventricle occurring just before the S1 sound. It may be heard in aortic stenosis, hypertrophic cardiomyopathy or HTN.
It coincides with the P wave on the ECG

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2
Q

What causes S3 - 3rd heart sound?

A

caused by diastolic filling of the ventricle
considered normal if < 30 years old (may persist in women up to 50 years old)
heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation

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3
Q

What is the first line investigation for stable angina?

A

Contrast-enhanced CT coronary angiogram

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4
Q

how is anginal chest pain defined?

A
  1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
  2. precipitated by physical exertion
  3. relieved by rest or GTN in about 5 minutes
    patients with all 3 features have typical angina
    patients with 2 of the above features have atypical angina
    patients with 1 or none of the above features have non-anginal chest pain
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5
Q

how is stable angina managed?

A

aspirin + statin
GTN
Beta blocker or CCB as first line
If CCB used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used
If CCB in combo with BB then use a longer-acting dihydropyridine calcium channel blocker (e.g. amlodipine, modified-release nifedipine)
If monotherapy does not work then add in the other
Then consider adding in a long actin nitrate, ivabradine nicorandil, ranolazine

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6
Q

what is Arrhythmogenic right ventricular cardiomyopathy?

A

a form of inherited cardiovascular disease which may present with syncope or sudden cardiac death. It is generally regarded as the second most common cause of sudden cardiac death in the young after hypertrophic cardiomyopathy.

Pathophysiology
inherited in an autosomal dominant pattern with variable expression
the right ventricular myocardium is replaced by fatty and fibrofatty tissue
around 50% of patients have a mutation of one of the several genes which encode components of desmosome

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6
Q

What is the JVP wave form

A

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

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7
Q

How does arrhythmogenic right ventricular cardiomyopathy present?

A

palpitations
syncope
sudden cardiac death

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8
Q

What investigations for Arrhythmogenic right ventricular cardiomyopathy and what do they show?

A

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

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9
Q

WHat is the management of arrhythmogenic right ventricular cardiomyopathy ?

A

drugs: sotalol is the most widely used antiarrhythmic
catheter ablation to prevent ventricular tachycardia
implantable cardioverter-defibrillator

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10
Q

WHat is Naxos disease?

A

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

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11
Q

what murmur is heard in ASD?

A

Ejection systolic murmur heard louder on inspiration

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12
Q

what causes ejection systolic murmurs

A

louder on expiration
aortic stenosis
hypertrophic obstructive cardiomyopathy

louder on inspiration
pulmonary stenosis
atrial septal defect

also: tetralogy of Fallot

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13
Q

What causes pansystolic murmur

A

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)

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14
Q

what causes a late systolic murmur

A

mitral valve prolapse
coarctation of aorta

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15
Q

what causes early diastolic murmur

A

aortic regurgitation (high-pitched and ‘blowing’ in character)
Graham-Steel murmur (pulmonary regurgitation, again high-pitched and ‘blowing’ in character)

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16
Q

What causes mid-late diastolic murmur?

A

mitral stenosis (‘rumbling’ in character)
Austin-Flint murmur (severe aortic regurgitation, again is ‘rumbling’ in character)

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17
Q

what causes a continuous machine-like murmur?

A

patent ductus arteriosus

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18
Q

how is DVT/PE investigated in pregnancy?

A

Suspected DVT - USS Doppler
PE - if DVT also suspected the USS doppler, if just PE - then the decision to perform a V/Q or CTPA should be taken at a local level after discussion with the patient and radiologist

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19
Q

what is the treatment of prinzmetal angina?

A

dihydropyridine calcium channel blocker
Felodipine

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20
Q

How is SVT managed and prevented?

A

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

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21
Q

What is given for SVT prevention in pregnancy?

A

Metoprolol

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22
Q

what is pulmonary capillary wedge pressure?

A

Pulmonary capillary wedge pressure (PCWP) is measured using a balloon tipped Swan-Ganz catheter which is inserted into the pulmonary artery. The pressure measured is similar to that of the left atrium (normally 6-12 mmHg).

One of the main uses of measuring the PCWP is determining whether pulmonary oedema is caused by either heart failure or acute respiratory distress syndrome.

In many modern ITU departments PCWP measurement has been replaced by non-invasive techniques.

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23
Q

why is an asymmetric dosing regimen of isosorbide mononitrate recommended?

A

An asymmetric dosing regimen would involve taking the morning dose as normal, then taking the second dose in the early afternoon. This allows a sufficiently long nitrate-free period and helps reduce tolerance.

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24
what is the mechanism of action of amiodarone?
he 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)
25
what are the monitoring requirements of amiodarone?
TFT, LFT, U&E, CXR prior to treatment TFT, LFT every 6 months
26
where do thiazide/thiazide like diuretics act?
inhibits sodium reabsorption by blocking the Na+-Clˆ’ symporter at the beginning of the distal convoluted tubule Potassium is lost as a result of more sodium reaching the collecting ducts.
27
What are the adverse effects of amiodarone use?
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
28
what are the common adverse effects of thiazide/thiazide like diuretics?
dehydration postural hypotension hypokalaemia - due to increased delivery of sodium to the distal part of the distal convoluted tubule → increased sodium reabsorption in exchange for potassium and hydrogen ions hyponatraemia hypercalcaemia the flip side of this is hypocalciuria, which may be useful in reducing the incidence of renal stones gout impaired glucose tolerance impotence Rare adverse effects thrombocytopaenia agranulocytosis photosensitivity rash pancreatitis
29
where do loop diuretics act?
Loop diuretics (furosemide, bumetanide) act by inhibiting the Na+/K+/2Cl- cotransporter in the thick ascending limb of the loop of Henle. This causes loss of water along with sodium chloride, potassium, calcium, and hydrogen ions.
30
what are the are the adverse effects of loop diuretics?
hypotension hyponatraemia hypokalaemia, hypomagnesaemia hypochloraemic alkalosis ototoxicity hypocalcaemia renal impairment (from dehydration + direct toxic effect) hyperglycaemia (less common than with thiazides) gout
31
what is pulmonary artery hypertension defined as?
defined as a resting mean pulmonary artery pressure of >= 20 mmHg
32
what are the features of pulmonary artery hypertension?
progressive exertional dyspnoea is the classical presentation other possible features include exertional syncope, exertional chest pain and peripheral oedema cyanosis right ventricular heave, loud P2, raised JVP with prominent 'a' waves, tricuspid regurgitation
33
How is pulmonary artery hypertension managed?
Treat underlying conditions Following this - acute vasodilator testing is central to deciding on the appropriate management strategy. If there is a positive response - oral calcium channel blockers If there is a negative response: prostacyclin analogues: treprostinil, iloprost endothelin receptor antagonists non-selective: bosentan selective antagonist of endothelin receptor A: ambrisentan phosphodiesterase inhibitors: sildenafil
34
what is acute vasodilator testing?
Acute vasodilator testing aims to decide which patients show a significant fall in pulmonary arterial pressure following the administration of vasodilators such as intravenous epoprostenol or inhaled nitric oxide
35
What are the causes of 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
36
what are the features of pericarditis?
chest pain: may be pleuritic. Is often relieved by sitting forwards other symptoms include a non-productive cough, dyspnoea and flu-like symptoms pericardial rub
37
what would ECG show in pericarditis?
the changes in pericarditis are often global/widespread, as opposed to the 'territories' seen in ischaemic events 'saddle-shaped' ST elevation PR depression: most specific ECG marker for pericarditis
38
WHat are the investigations in pericarditis?
ECG all patients with suspected acute pericarditis should have transthoracic echocardiography bloods inflammatory markers troponin: around 30% of patients may have an elevated troponin - this indicates possible myopericarditis
39
What is the management of pericarditis?
treat underlying cause avoid strenuous physical activity until resolution of symptoms NSAIDs and colchicine
40
when should pericarditis be managed in the hospital?
patients who have high-risk features such as fever > 38°C or elevated troponin should be managed as an inpatient
41
What happens to BP in pregnancy?
Falls in first half of pregnancy before rising to pre-pregnancy levels before term. During a healthy pregnancy, blood pressure will typically fall during the first half of pregnancy due to systemic vasodilation and increased blood volume. The systolic pressure tends to drop by 5-10 mmHg and the diastolic by as much as 10-15 mmHg. This decrease reaches its nadir between the mid-second and early third trimester, after which it gradually rises back towards baseline prepregnancy levels just before term.
42
what is the management of hypertension in pregnancy?
Labetalol oral nifedipine labetalol is contraindicated
43
what are the poor prognostic factors in infective endocarditis?
Staphylococcus aureus infection (see below) prosthetic valve (especially 'early', acquired during surgery) culture negative endocarditis low complement levels
44
what bacteria has the highest mortality in IE?
staphylococci - 30%
45
why are ACEi contraindicated in HOCM with left ventricular outflow tract obstruction
. ACE inhibitors can reduce afterload which may worsen the LVOT gradient
46
What are the characteristic signs of HOCM on echo
mitral regurgitation, systolic anterior motion of the anterior mitral valve leaflet, asymmetric hypertrophy
47
How is HOCM inherited
AD
48
How is HOCM managed
ABCDE Amiodarone Beta-blockers or verapamil for symptoms Cardioverter defibrillator Dual chamber pacemaker Endocarditis prophylaxis*
49
drugs to avoid in HOCM?
nitrates ACE-inhibitors inotropes
50
what is the pathophysiology of HOCM ?
the most common defects involve a mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C results in predominantly diastolic dysfunction left ventricle hypertrophy → decreased compliance → decreased cardiac output characterized by myofibrillar hypertrophy with chaotic and disorganized fashion myocytes ('disarray') and fibrosis on biopsy
51
What are the features of HOCM
exertional dyspnoea angina syncope - typically following exercise sudden death jerky pulse, large a waves, double apex beat systolic murmurs ejection systolic murmur: due to left ventricular outflow tract obstruction. Increases with Valsalva manoeuvre and decreases on squatting pansystolic murmur: due to systolic anterior motion of the mitral valve → mitral regurgitation
52
What are the ECG findings in HOCM
left ventricular hypertrophy non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen deep Q owaves atrial fibrillation may occasionally be seen
53
how long do you treat unprovoked PE for?
6 months
54
what is the mechanism of action of statins?
Statins inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis.
55
What are the adverse effects of statins
myopathy (myalgia, myositis, rhabdomyolysis, and asymptomatic raised creatine kinase) Liver impairment there is some evidence that statins may increase the risk of intracerebral haemorrhage in patients who've previously had a stroke. This effect is not seen in primary prevention. For this reason the Royal College of Physicians recommend avoiding statins in patients with a history of intracerebral haemorrhage
56
WHat increases the risk of statin-induced myopathy?
Risks factors for myopathy include advanced age, female sex, low body mass index and presence of multisystem disease such as diabetes mellitus. Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)
57
What are contraindications to statins
macrolides (e.g. erythromycin, clarithromycin) are an important interaction. Statins should be stopped until patients complete the course pregnancy
58
what conditions are associated with mitral valve prolapse?
coarr ngenital heart disease: PDA, ASD cardiomyopathy Turner's syndrome Marfan's syndrome, Fragile X hapseudoxanthoma elasticum Wolff-Parkinson White syndrome long-QT syndrome Ehlers-Danlos Syndrome polycystic kidney disease
59
what are the fetures of mitral prolapse?
patients may complain of atypical chest pain or palpitations mid-systolic click (occurs later if patient squatting) late systolic murmur (longer if patient standing) complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death
60
what are the features of aortic regurgitation
early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre collapsing pulse wide pulse pressure Quincke's sign (nailbed pulsation) De Musset's sign (head bobbing) mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
61
what are the side effects of ACEi
cough: occurs in around 15% of patients and may occur up to a year after starting treatment. Thought to be due to increased bradykinin levels angioedema: may occur up to a year after starting treatment hyperkalaemia first-dose hypotension: more common in patients taking diuretics
62
what are the cautions and contraindications when using ACEi
pregnancy and breastfeeding - avoid renovascular disease - significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis aortic stenosis - may result in hypotension patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day) - significantly increases the risk of hypotension hereditary or idiopathic angioedema
63
what is patent ductus arteriosus?
a form of congenital heart defect generally classed as 'acyanotic'. However, uncorrected can eventually result in late cyanosis in the lower extremities, termed differential cyanosis connection between the pulmonary trunk and descending aorta usually, the ductus arteriosus closes with the first breaths due to increased pulmonary flow which enhances prostaglandins clearance more common in premature babies, born at high altitude or maternal rubella infection in the first trimester
64
what are the features of PDA?
left subclavicular thrill continuous 'machinery' murmur large volume, bounding, collapsing pulse wide pulse pressure heaving apex beat
65
what is the management of PDA?
indomethacin or ibuprofen given to the neonate inhibits prostaglandin synthesis closes the connection in the majority of cases if associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair
66
what is Tirofiban?
Tirofiban is a glycoprotein (GP) IIb/IIIa receptor antagonist that works by inhibiting platelet aggregation. It does this by binding to the GP IIb/IIIa receptors on the surface of platelets, preventing fibrinogen from binding to these receptors and thus blocking platelet aggregation. This reduces thrombus formation in the coronary arteries and improves blood flow, making it an effective treatment for acute coronary syndrome.
67
what is the mechanism of action of ACEi?
inhibits the conversion angiotensin I to angiotensin II → decrease in angiotensin II levels → to vasodilation and reduced blood pressure → decrease in angiotensin II levels → reduced stimulation for aldosterone release → decrease in sodium and water retention by the kidneys
68
what is the renoprotective mechanism of ACEi?
angiotensin II constricts the efferent glomerular arterioles ACE inhibitors therefore lead to dilation of the efferent arterioles → reduced glomerular capillary pressure → decreased mechanical stress on the delicate filtration barriers of the glomeruli this is particularly important in diabetic nephropathy ACE inhibitors are activated by phase 1 metabolism in the liver
69
how do you manage patients taking warfarin who need emergency?
If surgery can wait for 6-8 hours - give 5 mg vitamin K IV If surgery can't wait - 25-50 units/kg four-factor prothrombin complex The guidance is to stop warfarin before elective or emergency surgery, so options 3 and 5 are incorrect Because this is emergency surgery, reversal of anticoagulation is necessary so option 2 is incorrect
70
what is the mechanism of action of warfarin?
mechanical heart valves target INR depends on the valve type and location mitral valves generally require a higher INR than aortic valves. second-line after DOACs: venous thromboembolism: target INR = 2.5, if recurrent 3.5 atrial fibrillation, target INR = 2.5
71
what are the features of ASD
ejection systolic murmur, fixed splitting of S2 embolism may pass from venous system to left side of heart causing a stroke
72
what are the types of ASD
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
73
why should verapamil not be used in VT ?
Verapamil should be avoided in this patient as it is contraindicated in VT due to the risk of causing significant hypotension, ventricular fibrillation and cardiac arrest. However, verapamil can be used safely in the management of supraventricular tachycardia (SVT).
74
what are the drugs routinely used in VT?
amiodarone: ideally administered through a central line lidocaine: use with caution in severe left ventricular impairment procainamide
75
which coronary artery is most likely to be affected if a patient presents with heart block post MI
The atrioventricular node is supplied by the posterior interventricular artery, which in the majority of patients is a branch of the right coronary artery. In the remainder of patients the posterior interventricular artery is supplied by the left circumflex artery.
76
what are the causes of palmar xanthoma?
remnant hyperlipidaemia may less commonly be seen in familial hypercholesterolaemia
77
what is eruptive xanthoma?
Eruptive xanthoma are due to high triglyceride levels and present as multiple red/yellow vesicles on the extensor surfaces (e.g. elbows, knees)
78
what are the causes of eruptive xanthoma?
familial hypertriglyceridaemia lipoprotein lipase deficiency
79
what are the causes of Tendon xanthoma, tuberous xanthoma, xanthelasma?
familial hypercholesterolaemia remnant hyperlipidaemia
80
what are the clinical features of aortic stenosis?
chest pain SOB syncope/presyncope murmur
81
what are the 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
82
what are the 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
83
how is aortic stenosis managed ?
if asymptomatic - observation symptomatic - valve replacement asymptomatic - but valvular gradient > 40 then consider surgery
84
what ate the complications of bicuspid aortic valve
aortic stenosis/regurgitation as above higher risk for aortic dissection and aneurysm formation of the ascending aorta
84
what congenital heart defect is associated with bicuspid aortic valve ?
coarctation of the aorta
85
what are the indications for ICD?
long QT syndrome hypertrophic obstructive cardiomyopathy previous cardiac arrest due to VT/VF previous myocardial infarction with non-sustained VT on 24 hr monitoring, inducible VT on electrophysiology testing and ejection fraction < 35% Brugada syndrome
86
what are the causes of prolonged PR interval?
idiopathic ischaemic heart disease digoxin toxicity hypokalaemia* rheumatic fever aortic root pathology e.g. abscess secondary to endocarditis Lyme disease sarcoidosis myotonic dystrophy
87
what are the features of aortic regurgitation?
early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre collapsing pulse wide pulse pressure Quincke's sign (nailbed pulsation) De Musset's sign (head bobbing) mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
88
what are causes of aortic regurgitation ?
rheumatic fever calcified valve disease connective tissue diseases e.g. rheumatoid arthritis/SLE Bicuspid aortic valve spondyarthropathies HTN Syphlis marfams Acute causes - IE, aortic dissection
89
what is the most specific marker of pericarditis on ECG?
PR depression Sadly shaped ST elevation is also seen but not as a specific marker as PR depression
90
what are the clinical features of pericarditis?
chest pain: may be pleuritic. Is often relieved by sitting forwards other symptoms include a non-productive cough, dyspnoea and flu-like symptoms pericardial rub
91
what are the signs of tricuspid regurgitation?
pan-systolic murmur prominent/giant V waves in JVP pulsatile hepatomegaly left parasternal heave
92
what is the PERC criteria?
Pulmonary embolism rule-out criteria (PERC Age > 50 HR > 110 O2 <94 previous DVT/PE recent surgery/trauma in the last 4 weeks haemoptysis unilateral leg swelling oestrogen use if all of the above are negative the post test probably of PE is < 2%
93
what are the 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
94
what are the 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
95
when is adenosine used?
used in haemodynamically stable patients with a narrow complex tachycardia
96
when is amioderone given in an arrest?
amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered. a further dose of amiodarone 150 mg should be given to patients who are in VF/pulseless VT after 5 shocks have been administered lidocaine used as an alternative if amiodarone is not available or a local decision has been made to use lidocaine instead
96
when is adrenaline given in an arrest?
adrenaline 1 mg as soon as possible for non-shockable rhythms during a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have restarted after the third shock repeat adrenaline 1mg every 3-5 minutes whilst ALS continues
97
what are the causes of IE?
staph aureus - most common, especially in IVDU Strep viridian - linked with poor dental hygiene coagulase-negative staph - caused by lines, common in patients post valve replacement strep bovis - colorectal cancer non-infective 0 SLE (Libman sacks), malignancy - mar antic endocarditis Culture negative causes prior antibiotic therapy Coxiella burnetii Bartonella Brucella HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
98
what ECG changes are commonly seen in athletes?
first degree AV block Incomplete RBBB isolated QRS voltage criteria for left ventricular hypertrophy
98
what does an ECG show in LBBB?
in LBBB there is a 'W' in V1 and a 'M' in V6
99
what does an ECG show in RBBB ?
in RBBB there is a 'M' in V1 and a 'W' in V6
100
what are the causes of LBBB?
LBBB is always pathological causes include: myocardial infarction diagnosing a myocardial infarction for patients with existing LBBB is difficult rhe Sgarbossa criteria can help with this - please see the link for more details hypertension aortic stenosis cardiomyopathy rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
101
what form of step is most associated with colorectal cancer?
Streptococcus gallolyticus is the subtype of Streptococcus bovis most linked with colorectal cancer
102
What are the radioactive substances used in nuclear cardiac imaging?
thallium technetium (99mTc) sestamibi: a coordination complex of the radioisotope technetium-99m with the ligand methoxyisobutyl isonitrile (MIBI), used in 'MIBI' or cardiac Single Photon Emission Computed Tomography (SPECT) scans fluorodeoxyglucose (FDG): used in Positron Emission Tomography (PET) scans radionuclide (technetium-99m) is injected intravenously- multigated acquisition scan - radionuclide angiography
102
Poor prognostic factors in HOCM?
Poor prognostic factors syncope family history of sudden death young age at presentation non-sustained ventricular tachycardia on 24 or 48-hour Holter monitoring abnormal blood pressure changes on exercise An increased septal wall thickness is also associated with a poor prognosis.
103
what is the renoprotective mechanism of ACEi?
**The renoprotective effects of ACE inhibitors are mediated through dilation of the glomerular efferent arteriole ** angiotensin II constricts the efferent glomerular arterioles ACE inhibitors therefore lead to dilation of the efferent arterioles → reduced glomerular capillary pressure → decreased mechanical stress on the delicate filtration barriers of the glomeruli this is particularly important in diabetic nephropathy
104
CHADSCASC score?
105
what pulse is seen in mixed aortic disease?
Bisferiens pulse
106
Eclampsia is defined as?
Eclampsia may be defined as the development of seizures in association pre-eclampsia. To recap, pre-eclampsia is defined as: condition seen after 20 weeks gestation pregnancy-induced hypertension proteinuria
107
Management of Eclampsia?
Magnesium sulphate is used to both prevent seizures in patients with severe pre-eclampsia and treat seizures once they develop. Guidelines on its use suggest the following: should be given once a decision to deliver has been made in eclampsia an IV bolus of 4g over 5-10 minutes should be given followed by an infusion of 1g / hour urine output, reflexes, respiratory rate and oxygen saturations should be monitored during treatment respiratory depression can occur: calcium gluconate is the first-line treatment for magnesium sulphate induced respiratory depression treatment should continue for 24 hours after last seizure or delivery (around 40% of seizures occur post-partum) Other important aspects of treating severe pre-eclampsia/eclampsia include fluid restriction to avoid the potentially serious consequences of fluid overload
108
What is Rheumatic fever?
Rheumatic fever develops following an immunological reaction to a recent (2-4 weeks ago) Streptococcus pyogenes infection.
109
Pathogenesis of rheumatic fever?
Streptococcus pyogenes infection → activation of the innate immune system leading to antigen presentation to T cells B and T cells produce IgG and IgM antibodies and CD4+ T cells are activated there is then a cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry the cell wall of Streptococcus pyogenes includes M protein, a virulence factor that is highly antigenic. It is thought that the antibodies against M protein cross-react with myosin and the smooth muscle of arteries this response leads to the clinical features of rheumatic fever Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever
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what histological finding in rheumatic heart disease?
Aschoff bodies are granulomatous nodules found in rheumatic heart fever
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Diagnostic criteria for rheumatic heart disease?
Diagnosis is based on evidence of recent streptococcal infection accompanied by: 2 major criteria 1 major with 2 minor criteria 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: this is often a late feature polyarthritis carditis and valvulitis (eg, pancarditis) The latest iteration of the Jones criteria (published in 2015) state that rheumatic carditis cannot be based on pericarditis or myocarditis alone and that there must be evidence of endocarditis (the clinical correlate of which is valvulitis which manifests as a regurgitant murmur) subcutaneous nodules Minor criteria raised ESR or CRP pyrexia arthralgia (not if arthritis a major criteria) prolonged PR interval
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what is associated with coarctation of the aorta?
Turner's syndrome bicuspid aortic valve berry aneurysms neurofibromatosis
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Features of coarctation of the aorta?
Features 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 children ## Footnote The most common type of coarctation of the aorta seen in adults is the postductal variety, i.e. the aortic narrowing is distal to the ductus arteriosus. This means that the upper limb blood pressure is greater than that in the lower limbs as the narrowing occurs after the left subclavian artery branches from the aorta.
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Target INR for mechanical heart valve?
Target INR aortic: 3.0 mitral: 3.5
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features of cholesterol emboli?
Overview cholesterol emboli may break off causing renal disease the majority of cases are secondary to vascular surgery or angiography. Other causes include severe atherosclerosis, particularly in large arteries such as the aorta Features eosinophilia purpura renal failure livedo reticularis
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what drug should be avoided in V T?
Verapamil should never be given to a patient with a broad complex tachycardia as it may precipitate ventricular fibrillation in patients with ventricular tachycardia.
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what murmurs increase in intestity and decrease in intensity with handgrip?
**Increased Intensity:** Aortic and Mitral Regurgitation: The increased afterload caused by handgrip makes it harder for the heart to pump blood, leading to increased backflow and a louder murmur. Ventricular Septal Defect: Similar to regurgitation, the increased afterload increases the amount of blood flowing through the defect, resulting in a louder murmur. ** Decreased Intensity:** Hypertrophic Obstructive Cardiomyopathy (HOCM): Handgrip increases afterload, which reduces the obstruction in the left ventricular outflow tract, thereby decreasing the intensity of the murmur. Mitral Valve Prolapse (MVP): Handgrip increases afterload, which reduces the severity of mitral regurgitation, leading to a decrease in murmur intensity and a delay in the timing of the mid-systolic click.
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Multifocal atiral tachycardia - management?
Multifocal atrial tachycardia (MAT) may be defined as a irregular cardiac rhythm caused by at least three different sites in the atria, which may be demonstrated by morphologically distinctive P waves. It is more common in elderly patients with chronic lung disease, for example COPD Management correction of hypoxia and electrolyte disturbances rate-limiting calcium channel blockers are often used first-line cardioversion and digoxin are not useful in the management of MAT