Cardiology Flashcards
(146 cards)
1
Q
What are the most common valves which need replacing?
A
The most common valves which need replacing are the aortic and mitral valve.
2
Q
What are the two options for valve replacement?
A
Biological (Bioprosthetic) and mechanical
Biological is usually bovine or porcine in origin
3
Q
What are the advantages and disadvantages of biological valves?
A
Major disadvantage is structural deterioration and calcification over time. Most older patients ( > 65 years for aortic valves and > 70 years for mitral valves) receive a bioprosthetic valve
Long-term anticoagulation not usually needed. Warfarin may be given for the first 3 months depending on patient factors. Low-dose aspirin is given long-term.
4
Q
What are the advantages and disadvantages of mechanical valves?
A
Mechanical valves have a low failure rate
Major disadvantage is the increased risk of thrombosis meaning long-term anticoagulation is needed.
5
Q
What ongoing anticoagulation management is used in mechanical valves?
A
Warfarin
Asprin- if ischaemic heart disease
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
6
Q
What ongoing anticoagulation management is used in biological valves?
A
Long-term anticoagulation not usually needed. Warfarin may be given for the first 3 months depending on patient factors. Low-dose aspirin is given long-term.
7
Q
What are Mechanical valves - target INR?
A
Mechanical valves - target INR:
aortic: 3.0
mitral: 3.5
8
Q
NICE guidelines (2021) suggest which patients with AF should not have rate control as first-line?
A
1.A reversible cause for their AF
2.New onset atrial fibrillation (within the last 48 hours)
3.Heart failure caused by atrial fibrillation
4.Symptoms despite being effectively rate controlled
9
Q
What are the two scenarios where cardioversion may be used in atrial fibrillation?
A
- electrical cardioversion as an emergency if the patient is haemodynamically unstable
- electrical or pharmacological cardioversion as an elective procedure where a rhythm control strategy is preferred.
10
Q
What are the principles for AF management?
A
11
Q
Rheumatic fever develops following infection with what?
A
Streptococcus pyogenes.
12
Q
What is the diagnosis of rheumatic fever based on?
A
Diagnosis is based on evidence of recent streptococcal infection accompanied by:
2 major criteria
1 major with 2 minor criteria
13
Q
What is the major and minor criteria of the diagnosis of rheumatic fever?
A
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
14
Q
What is the evidence of recent streptococcal infection
A
Evidence of recent streptococcal infection
raised or rising streptococci antibodies,
positive throat swab
positive rapid group A streptococcal antigen test
15
Q
What is the management of rheumatic fever?
A
Management
Outline of management
antibiotics: oral penicillin V
anti-inflammatories: NSAIDs are first-line
treatment of any complications that develop e.g. heart failure
16
Q
What is the management of SVTs?
A
Management of supraventricular tachycardia in patients without life-threatening features involves a stepwise approach, trying each step to see whether it works before moving on.
Step 1: Vagal manoeuvres
Step 2: Adenosine
Step 3: Verapamil or a beta blocker
Step 4: Synchronised DC cardioversion
Patients with life-threatening features, such as loss of consciousness (syncope), heart muscle ischaemia (e.g., chest pain), shock or severe heart failure, are treated with synchronised DC cardioversion under sedation or general anaesthesia. Intravenous amiodarone is added if initial DC shocks are unsuccessful.
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
17
Q
What is Wolff-Parkinson White (WPW) syndrome?
A
Wolff-Parkinson White (WPW) syndrome is caused by a congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT). As the accessory pathway does not slow conduction AF can degenerate rapidly to VF.
18
Q
What are the ECG features of WPW?
A
Possible ECG features include:
short PR interval
wide QRS complexes with a slurred upstroke - ‘delta wave’
left axis deviation if right-sided accessory pathway
in the majority of cases, or in a question without qualification, Wolff-Parkinson-White syndrome is associated with left axis deviation
right axis deviation if left-sided accessory pathway
Differentiating between type A and type B
type A (left-sided pathway): dominant R wave in V1
type B (right-sided pathway): no dominant R wave in V1
19
Q
What are other conditons asscoiated with WPW?
A
Associations of WPW
HOCM
mitral valve prolapse
Ebstein’s anomaly
thyrotoxicosis
secundum ASD
20
Q
What is the management of WPW?
A
Management
definitive treatment: radiofrequency ablation of the accessory pathway
medical therapy: sotalol***, amiodarone, flecainide
sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation
Patients with Wolff-Parkinson-White syndrome (pre-excitation syndrome) with possible atrial arrhythmias (e.g., atrial fibrillation or atrial flutter) should not have adenosine, verapamil or a beta blocker, as these block the atrioventricular node, promoting conduction of the atrial rhythm through the accessory pathway into the ventricles, causing potentially life-threatening ventricular rhythms. Sometimes it can be difficult to distinguish this from SVT, so the involvement of experienced seniors is essential. In this scenario, the usual management is procainamide (which does not block the AV node) or electrical cardioversion (if unstable).
21
Q
What are the complications of MI?
A
DREAD
D – Death- cardiac arrest due to VF
R – Rupture of the heart septum or papillary muscles
E – “oEdema” (heart failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome
Cardiogenic shock
If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock
Chronic heart failure
As described above, if the patient survives the acute phase their ventricular myocardium may be dysfunctional resulting in chronic heart failure. Loop diuretics such as furosemide will decrease fluid overload. Both ACE-inhibitors and beta-blockers have been shown to improve the long-term prognosis of patients with chronic heart failure.
Tachyarrhythmias
Ventricular fibrillation, as mentioned above, is the most common cause of death following a MI. Other common arrhythmias including ventricular tachycardia.
Bradyarrhythmias
Atrioventricular block is more common following inferior myocardial infarctions.
Pericarditis
Pericarditis in the first 48 hours following a transmural MI is common (c. 10% of patients). The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram.
Dressler’s syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.
Left ventricular aneurysm
The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.
Left ventricular free wall rupture
This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.
Ventricular septal defect
Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients. Features: acute heart failure associated with a pan-systolic murmur. An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion. Urgent surgical correction is needed.
Acute mitral regurgitation
More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle. Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard. Patients are treated with vasodilator therapy but often require emergency surgical repair.
22
Q
What is Dresslers syndrome?
A
Dressler’s syndrome is also called post-myocardial infarction syndrome. It usually occurs around 2 – 3 weeks after an acute myocardial infarction. It is caused by a localised immune response that results in inflammation of the pericardium, the membrane that surrounds the heart (pericarditis).
23
Q
Presentation, Diagnosis, management of dresslers syndrome
A
It presents with pleuritic chest pain, low-grade fever and a pericardial rub on auscultation. A pericardial rub is a rubbing, scratching sound that occurs alongside the heart sounds. It can cause a pericardial effusion and rarely a pericardial tamponade (where the fluid constricts the heart and inhibits function).
A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).
Management is with NSAIDs (e.g., aspirin or ibuprofen) and, in more severe cases, steroids (e.g., prednisolone). Pericardiocentesis may be required to remove fluid from around the heart, if there is a significant pericardial effusion.
24
Q
what is acute pericarditis?
A
Acute pericarditis is a condition referring to inflammation of the pericardial sac, lasting for less than 4-6 weeks.
25
What are the causes of pericarditis?
Idiopathic (no underlying cause)
Infection (e.g., tuberculosis, HIV, coxsackievirus, Epstein–Barr virus and other viruses)
Autoimmune and inflammatory conditions (e.g., systemic lupus erythematosus and rheumatoid arthritis)
Injury to the pericardium (e.g., after myocardial infarction, open heart surgery or trauma)
Uraemia (raised urea) secondary to renal impairment
Cancer (lung cancer, breast cancer)
Medications (e.g., methotrexate)
hypothyroidism
radiotherapy
26
Presentation of pericarditis
Two key presenting features should make you think of pericarditis:
Chest pain
Low-grade fever
The chest pain is:
Sharp
Central/anterior
Worse with inspiration (pleuritic)
Worse on lying down
Better on sitting forward
Pericardial friction rub on auscultation is a key examination finding. A pericardial rub is a rubbing, scratching sound that occurs alongside the heart sounds.
other symptoms include a non-productive cough, dyspnoea and flu-like symptoms
27
What are the investigations for pericarditis and ECG changes?
Investigations
Blood tests show raised inflammatory markers (white blood cells, CRP and ESR).
ECG changes include:
Saddle-shaped ST-elevation
PR depression
Echocardiogram can be used to diagnose a pericardial effusion.
all patients with suspected acute pericarditis should have transthoracic echocardiography
28
Management of pericarditis
Management
-Non-steroidal anti-inflammatory drugs (NSAIDs) are the mainstay of treatment (e.g., aspirin or ibuprofen)
-Colchicine (taken longer-term, e.g., 3 months, to reduce the risk of recurrence)
Steroids may be used second-line, in recurrent cases or associated with inflammatory conditions (e.g., rheumatoid arthritis)
Underlying causes, such as tuberculosis and renal failure, should be treated appropriately.
Pericardiocentesis may be required to remove fluid from around the heart if there is a significant pericardial effusion or tamponade.
the majority of patients can be managed as outpatients
patients who have high-risk features such as fever > 38°C or elevated troponin should be managed as an inpatient
treat any underlying cause
most patients however will have pericarditis secondary to viral infection, meaning no specific treatment is indicated
strenuous physical activity should be avoided until symptom resolution and normalisation of inflammatory markers
a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis
until symptom resolution and normalisation of inflammatory markers (usually 1-2 weeks) followed by tapering of dose recommended over
29
Principles of diagnosing PE
30
The NICE guidelines (2021) recommend for anticoagulation in AF
The NICE guidelines (2021) recommend for anticoagulation:
Direct-acting oral anticoagulants (DOACs) first-line
Warfarin second-line, if DOACs are contraindicated
CHA2DS2-VASc is a tool for assessing whether a patient with atrial fibrillation should start anticoagulation. It is a list of risk factors that increase the likelihood of a stroke. The higher the score, the higher the risk of developing a stroke or TIA.
CHA2DS2-VASc is a mnemonic for the factors that score a point:
C – Congestive heart failure
H – Hypertension
A2 – Age above 75 (scores 2)
D – Diabetes
S2 – Stroke or TIA previously (scores 2)
V – Vascular disease
A – Age 65 – 74
S – Sex (female)
NICE (2021) recommends, based on the CHA2DS2-VASc score:
0 – no anticoagulation
1 – consider anticoagulation in men (women automatically score 1)
2 or more – offer anticoagulation
Aspirin alone is not used for stroke prevention in atrial fibrillation
31
What is the first line treatment for VT?
IV amiodarone
32
what is the treatment for Polymorphic ventricular tachycardia, such as torsades de pointes?
IV magnesium
33
Ejection systolic murmur is classically seen in?
Aortic stenosis
34
Describe the murmur in aortic stenosis
Aortic stenosis causes an ejection-systolic, high-pitched murmur due to the high blood flow velocity through the aortic valve. This has a crescendo-decrescendo character due to the speed of blood flow across the value during the different periods of systole. Flow during systole is slowest at the start and end and fastest in the middle.
The murmur radiates to the carotids as the turbulence continues into the neck.
35
What are the clinical signs and features of aortic stenosis?
Clinical features of symptomatic disease
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
Other signs of aortic stenosis:
Thrill in the aortic area on palpation
Slow rising pulse
Narrow pulse pressure (the difference between systolic and diastolic blood pressure)
Exertional syncope (lightheadedness and fainting when exercising) due to difficulty maintaining a good flow of blood to the brain
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
36
Causes of aortic stenosis
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
37
Management of aortic stenosis
Management
if asymptomatic then observe the patient is a general rule
if symptomatic then valve replacement
if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
options for aortic valve replacement (AVR) include:
surgical AVR is the treatment of choice for young, low/medium operative risk patients. Cardiovascular disease may coexist. For this reason, an angiogram is often done prior to surgery so that the procedures can be combined
transcatheter AVR (TAVR) is used for patients with a high operative risk
balloon valvuloplasty
may be used in children with no aortic valve calcification
in adults limited to patients with critical aortic stenosis who are not fit for valve replacement
38
What is acute coronary syndrome?
Acute coronary syndrome (ACS) is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery. When a thrombus forms in a fast-flowing artery, it is formed mainly of platelets. This is why antiplatelet medications such as aspirin, clopidogrel and ticagrelor are the mainstay of treatment.
39
What is the classification/types of acute coronary syndrome
ST-elevation myocardial infarction (STEMI): ST-segment elevation + elevated biomarkers of myocardial damage
non ST-elevation myocardial infarction (NSTEMI): ECG changes but no ST-segment elevation + elevated biomarkers of myocardial damage
unstable angina
40
What is the presentation of ACS?
Acute coronary syndrome typically presents with central, constricting chest pain.
The chest pain is often associated with:
Pain radiating to the jaw or arms
Nausea and vomiting
Sweating and clamminess
A feeling of impending doom
Shortness of breath
Palpitations
41
Who is at risk of silent MI?
Diabetics
42
What is the initial management of ACS?
MONA
Morphine
Oxygen
Nitrates
Aspirn
Common management of all patients with ACS
Initial drug therapy
aspirin 300mg
oxygen should only be given if the patient has oxygen saturations < 94% in keeping with British Thoracic Society oxygen therapy guidelines
morphine should only be given for patients with severe pain
previously IV morphine was given routinely
evidence, however, suggests that this may be associated with adverse outcomes
nitrates
can be given either sublingually or intravenously
useful if the patient has ongoing chest pain or hypertension
should be used in caution if patient hypotensive
43
What is the management of STEMI?
44
what Further antiplatelet prior to PCI is given
this is termed 'dual antiplatelet therapy', i.e. aspirin + another drug
if the patient is not taking an oral anticoagulant: prasugrel
if taking an oral anticoagulant: clopidogrel
45
What is the drug therapy given during PCI?
Drug therapy during PCI
patients undergoing PCI with radial access:
unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus
patients undergoing PCI with femoral access:
bivalirudin with bailout GPI
46
When should ECG be repeated after Fibrinolysis for STEMI
An ECG should be repeated after 60-90 minutes to see if the ECG changes have resolved. If patients have persistent myocardial ischaemia following fibrinolysis then PCI should be considered.
47
What is the management of NSTEMI
48
What are the medications for secondary prevention of MI?
Medication for secondary prevention can be remembered with the “6 A’s” mnemonic:
Aspirin 75mg once daily indefinitely
Another Antiplatelet (e.g., ticagrelor or clopidogrel) for 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril) titrated as high as tolerated
Atenolol (or another beta blocker – usually bisoprolol) titrated as high as tolerated
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
49
How is blood pressure classified?
50
How is hypertension diagnosed?
51
what should be given to patients who are in VF/pulseless VT after 3 shocks have been administered?
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
52
Infective endocarditis in intravenous drug users most commonly affects which valve?
Tricuspid valve
53
What is the most commonly affected valve overall?
Mitral valve
54
Early diastolic murmur is classically seen in
Aortic regurgitation
55
What are the causes of aortic regurgitation
It can be caused either by disease of the aortic valve or by distortion or dilation of the aortic root and ascending aorta.
56
What are 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
57
Management of Aortic regurgitation
Management
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
58
Acute coronary syndrome may present with atypical chest pain especially in which patients
female patients
59
Pathophysiology of Ischaemic heart disease
initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia
this results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large 'foam cells'. As these macrophages die the result can further propagate the inflammatory process.
smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque
60
Complications of atherosclerosis
Once a plaque has formed a number of complications can develop:
the plaque forms a physical blockage in the lumen of the coronary artery. This may cause reduced blood flow and hence oxygen to the myocardium, particularly at times of increased demand, resulting clinically in angina
the plaque may rupture, potentially causing a complete occlusion of the coronary artery. This may result in a myocardial infarction
61
What causes angina?
Gradual narrowing, resulting in less blood and therefore oxygen reaching the myocardium at times of increased demand. This results in angina, i.e. chest pain due to insufficient oxygen reaching the myocardium during exertion
62
Modifiable and nonmodifiable risk factors of a patient developing ischaemic heart disease
63
correlation between ECG changes and coronary territories:
64
What is aortic dissection?
Aortic dissection is a rare but serious cause of chest pain.
Pathophysiology
tear in the tunica intima of the wall of the aorta
65
What are the features of aortic dissection?
Features:
chest/back pain
typically severe and 'sharp', 'tearing' in nature
pain is typically maximal at onset
classically chest pain is more common in type A dissection and upper back pain is more common in type B dissection. However, there is considerable overlap and both chest and back pain are present in many patients
pulse deficit
weak or absent carotid, brachial, or femoral pulse
variation (>20 mmHg) in systolic blood pressure between the arms
aortic regurgitation
hypertension
other features may result from the involvement of specific arteries. For example:
coronary arteries → angina
spinal arteries → paraplegia
distal aorta → limb ischaemia
the majority of patients have no or non-specific ECG changes. In a minority of patients, ST-segment elevation may be seen in the inferior leads
66
What is the classification of aortic dissection?
Classification
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
67
What are the associations of aortic dissection?
Associations
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
68
Broad complex tachycardia following a myocardial infarction is almost always due to...
Broad complex tachycardia following a myocardial infarction is almost always due to ventricular tachycardia.
69
What is the management of angina?
The management of stable angina comprises lifestyle changes, medication, percutaneous coronary intervention and surgery. NICE produced guidelines in 2011 covering the management of stable angina
Medication
all patients should receive aspirin and a statin in the absence of any contraindication
sublingual glyceryl trinitrate to abort angina attacks
NICE recommend using either a beta-blocker or a calcium channel blocker first-line based on 'comorbidities, contraindications and the person's preference'
if a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used
if used in combination with a beta-blocker then use a longer-acting dihydropyridine calcium channel blocker (e.g. amlodipine, modified-release nifedipine)
remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)
if there is a poor response to initial treatment then medication should be increased to the maximum tolerated dose (e.g. for atenolol 100mg od)
if a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa
if a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs:
a long-acting nitrate
ivabradine
nicorandil
ranolazine
if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG
70
What is the most common cause of mitral stenosis
rheumatic fever
71
which murmur can present with heamoptisis?
The patient presents with a mid-diastolic low-pitched rumbling murmur which is characteristic of mitral stenosis. Mitral stenosis may present with haemoptysis due to increased pressures causing rupture of pulmonary vessels.
72
'f pharmacological cardioversion has been agreed on clinical and resource grounds for new-onset atrial fibrillation, offer:
flecainide or amiodarone if there is no evidence of structural or ischaemic heart disease or
amiodarone if there is evidence of structural heart disease.'
73
which beta blocker causes QT prolongation
satolol
74
What are the side effects of adenosine?
Due to its vasodilatory effects can cause, flushing nausea, sweating, bronchospasm and also chest pain. Chest pain can be a particularly worrying symptom for patients who already know they have a problem with their heart, and therefore patients should be warned about this before administering adenosine.
75
What is becks triad?
The hallmark signs of cardiac tamponade, collectively referred to as Beck's triad, include hypotension, elevated jugular venous pressure (JVP), and diminished heart sounds.
76
What are some features of cardiac tamponade?
Other features:
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
77
What are the key differences between constrictive pericarditis and cardiac tamponade
78
what should Patients taking warfarin avoid ?
Patients taking warfarin should avoid foods high in vitamin K, such as sprouts, spinach, kale and broccoli
79
Warfarin Mechanism of Action
Inhibition of Vitamin K Epoxide Reductase (VKOR):
Warfarin primarily inhibits the enzyme Vitamin K epoxide reductase (VKOR).
VKOR is responsible for converting vitamin K epoxide back into its active form (vitamin K hydroquinone) in the liver.
Vitamin K is essential for the synthesis of several coagulation factors (clotting factors) in the liver, specifically Factors II (prothrombin), VII, IX, and X, as well as the anticoagulant proteins C and S.
80
What is Coarctation of the aorta?
Coarctation of the aorta describes a congenital narrowing of the descending aorta. It is more common in males, despite an association with Turner's syndrome.
81
How does Coarctation of the aorta present in new borns?
This patient has presented with acute circulatory collapse at 2 days of age. This is typical of coarctation of the aorta. This is because the duct is supplying blood flow to the descending aorta, but when the duct closes at 2 days of age, blood flow becomes cut off. Hence the blood pressure drops in the lower limbs, and a murmur is often heard on the left side under the left clavicle and over the left scapula as in this case.
82
What are the 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
83
What are the associations of Coarctation of the aorta?
Associations
Turner's syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis
84
What are the ECG changes in posterior MIs?
ST depression and tall R waves in the anterior leads.
84
What is the management of bradycardia?
84
What dose of adrenaline should be given during a cardiac arrest?
1mg
According to the Resuscitation Council UK guidelines, during a cardiac arrest, 1 mg of adrenaline should be administered intravenously or intraosseously every 3-5 minutes during cardiopulmonary resuscitation (CPR). Adrenaline works by increasing coronary and cerebral blood flow during CPR. It achieves this by stimulating alpha-adrenergic receptors, which results in vasoconstriction.
85
What is the management of PEs?
apixaban or rivaroxaban (both DOACs) should be offered first-line following the diagnosis of a PE
instead of using low-molecular weight heparin (LMWH)
if neither apixaban or rivaroxaban are suitable then either LMWH followed by dabigatran or edoxaban OR LMWH followed by a vitamin K antagonist (VKA, i.e. warfarin)
if the patient has active cancer
if renal impairment is severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA
if the patient has antiphospholipid syndrome (specifically 'triple positive' in the guidance) then LMWH followed by a VKA should be used
Length of anticoagulation
all patients should have anticoagulation for at least 3 months
continuing anticoagulation after this period is partly determined by whether the VTE was provoked or unprovoked
a provoked VTE is due to an obvious precipitating event e.g. immobilisation following major surgery. The implication is that this event was transient and the patient is no longer at increased risk
an unprovoked VTE occurs in the absence of an obvious precipitating event, i.e. there is a possibility that there are unknown factors (e.g. mild thrombophilia) making the patient more at risk from further clots
if the VTE was provoked the treatment is typically stopped after the initial 3 months (3 to 6 months for people with active cancer)
if the VTE was unprovoked then treatment is typically continued for up to 3 further months (i.e. 6 months in total)
86
What is the management of PE with haemodynamic instability?
Thrombolysis
thrombolysis is now recommended as the first-line treatment for massive PE where there is circulatory failure (e.g. hypotension)
other invasive approaches should be considered where appropriate facilities exist
alteplase?
87
What can be used to reverse bleeding on dabigatran?
idarucizumab
88
What drugs are used in rate control in AF?
Agents used to control rate in patients with atrial fibrillation
beta-blockers( not satalolol)
a common contraindication for beta-blockers is asthma
calcium channel blockers (diltiazem/verapamil)
digoxin
89
What is the treatment for type 2 heart block?
pacemaker
90
What is the most common cause of bisferiens pulse?
The most common causes of a bisferiens pulse are mixed aortic valve disease (i.e. aortic regurgitation and stenosis) and hypertrophic obstructive cardiomyopathy (HOCM).
91
What is the blood pressure target for type 2 diabetics?
< 140/90 mmHg
92
What is the blood pressure target for type 1 diabetics?
Intervention levels for recommending blood pressure management should be 135/85 mmHg unless the adult with type 1 diabetes has albuminuria or 2 or more features of metabolic syndrome, in which case it should be 130/80 mmHg
93
What type of drugs should not be used in uncomplicated hypertension and why?
The routine use of beta-blockers in uncomplicated hypertension should be avoided, particularly when given in combination with thiazides, as they may cause insulin resistance, impair insulin secretion and alter the autonomic response to hypoglycaemia.
94
Incases of hypothermia causing cardiac arrest what should be the management?
In cases of hypothermia causing cardiac arrest, defibrillation is less effective and only 3 shocks should be administered before the patient is rewarmed to 30 degrees centigrade
95
What is Raynaud's phenomenon?
discolouration of extremities with cold exposure
96
In Raynaud's phenomenon with extremity ischaemia think...
Buerger's disease (or thromboangiitis obliterans) is a small and medium vessel vasculitis strongly associated with smoking. It causes Raynaud's phenomenon (discolouration of extremities with cold exposure) and extremity ischemia leading to intermittent claudication (pain in legs which occurs during exercise and is relieved by rest).
97
Buerger's disease is strongly associated with what?
Buerger's disease (also known as thromboangiitis obliterans) is a small and medium vessel vasculitis that is strongly associated with smoking.
98
What is the management of a patient with AF + an acute stroke ?
Management
following a stroke or TIA it is obviously important to exclude a haemorrhage before starting any anticoagulation or antiplatelet therapy
for longer-term stroke prevention, NICE recommend warfarin or a direct thrombin or factor Xa inhibitor
the timing of when to start depends on whether it is a TIA or stroke
following a TIA, anticoagulation for AF should start immediately once imaging has excluded haemorrhage
in acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks. Antiplatelet therapy should be given in the intervening period. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed
99
What is the management for aortic dissection?
Aortic dissection
type A - ascending aorta - control BP (IV labetalol) + surgery
type B - descending aorta - control BP(IV labetalol)
A type B aortic dissection is one that occurs distal to the left subclavian origin. These are generally managed with supportive treatment and blood pressure control to prevent progression. According to BMJ Best Practice 'surgery in this group is reserved for those with end-organ malperfusion, persistent pain, rapid aneurysmal degeneration, or rupture'.
100
What is the investigation of choice for aortic dissection?
CT angiography of the chest, abdomen and pelvis is the investigation of choice
suitable for stable patients and for planning surgery
a false lumen is a key finding in diagnosing aortic dissection
101
What are key pointers in a patient history for aortic dissection?
Key pointers in the history are:
Demographics: aortic dissections typically present in males in the sixth decade of life;
Cardiovascular risk: he is hypertensive, and an ex-smoker with a significant pack year history;
Past medical history: he has pectus excavatum and a tall stature, which could point towards Marfan's syndrome, for whom aortic dissections are associated;
Characteristics of pain: Aortic dissections are often described as sudden-onset, with peak severity from the start. In contrast, myocardial infarctions typically become worse with time. The dissection can sometimes occur with a rise in intrathoracic pressure, such as heavy lifting. The pain can radiate to the back between the shoulder blades and is described as 'sharp' or 'ripping/tearing'.
102
What are key pointers in a patient examination for aortic dissection?
Key pointers in the examination and investigations are:
Weak pulses - as blood isn't adequately flowing through the aorta to the peripheries;
Crescendo diastolic murmurs can arise from aortic incompetence causing regurgitation, which can occur in ascending aorta (type A) dissections;
A difference in blood pressure readings between the arms is a classic finding, along with hypertension - a risk factor for dissection;
ST depression on ECG is common in aortic dissection. A normal troponin essentially rules out myocardial ischaemia, but this can rise in the face of dissection affecting the aortic root and blood supply to the coronary arteries.
One of the differentials for a widened mediastinum on chest X-ray is aortic dissection. This is because extra blood is filling the aortic wall through the defect.
103
After starting an ACE inhibitor, significant renal impairment may occur if the patient has undiagnosed....
bilateral renal artery stenosis
104
The ECG shows complete disassociation between the atria and ventricles.
What coronary artery is most likely to have been affected?
right coronary artery
104
What Antibiotic prohylaxis is given to prevent infective endocarditis for dental or other procedures?
Antibiotic prohylaxis to prevent infective endocarditis is not routinely recommended in the UK for dental and other procedures
104
What is the most common cause of mitral stenosis?
rheumatic fever
105
According to NICE Guidelines, what Q risk score would justify the prescription of a statin
Statins should be given to patients with a 10-year cardiovascular risk >= 10%
105
What is typical and atypical chest pain?
'Typical' chest pain is defined by any chest discomfort that meets the 3 criteria listed by the NICE guideline 2016. Atypical chest pain is defined by any chest discomfort that meets the 2 of 3 criteri
Important for meLess important
Her chest pain is atypical as it only meets 2 out of the 3 criteria of stable angina.
Her chest pain is described as sharp (rather than constricting)
Her chest pain may be precipitated by physical exertion
Her chest pain is relieved by GTN spray within 5 minutes
patients with 1 or none of the above features have non-anginal chest pain
105
Poorly controlled hypertension, already taking a calcium channel blocker...
Poorly controlled hypertension, already taking a calcium channel blocker - add an ACE inhibitor or an angiotensin receptor blocker or a thiazide-like diuretic-indapamide
Adding bendroflumethiazide in addition to amlodipine is incorrect. Bendroflumethiazide is a thiazide diuretic and an easy point of confusion. Only thiazide-like diuretics, such as indapamide, are recommended in the next step of the algorithm.
106
Give two examples of loop diuretics and what is their mechanism of action?
Furosemide and bumetanide are loop diuretics that act by inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl. There are two variants of NKCC; loop diuretics act on NKCC2, which is more prevalent in the kidneys.
107
What are the indications for loop diuretics?
heart failure: both acute (usually intravenously) and chronic (usually orally)
resistant hypertension, particularly in patients with renal impairment
108
What are the adverse effects of loop diuretics?
Adverse effects
hypotension-Loop diuretics cause a significant loss of sodium and water (diuresis), reducing blood volume and cardiac output. This reduction in circulating blood volume can lead to hypotension
hyponatraemia-Loop diuretics cause sodium loss by inhibiting its reabsorption in the loop of Henle. If the kidneys are unable to compensate by increasing sodium retention in other parts of the nephron, hypovolemia and water retention can occur, leading to a dilutional hyponatraemia
hypokalaemia-The Na+/K+/2Cl- cotransporter in the loop of Henle is responsible for the reabsorption of sodium, potassium, and chloride. When this transporter is inhibited, sodium stays in the tubule and increases distal sodium delivery to the distal convoluted tubule (DCT) and collecting duct. This stimulates aldosterone release, which increases potassium excretion in exchange for sodium in the collecting ducts.
hypomagnesaemia-Like potassium, magnesium is reabsorbed in the loop of Henle via a similar transport mechanism. Inhibition of the Na+/K+/2Cl- cotransporter by loop diuretics leads to reduced magnesium reabsorption.
hypochloraemic alkalosis-Loop diuretics increase the excretion of chloride and sodium. As the body loses sodium and chloride, the kidneys may compensate by retaining bicarbonate (via aldosterone and RAAS activation), resulting in an alkalotic state (higher blood pH).
ototoxicity-Ototoxicity may be related to the drug's effect on the renal tubules and electrolyte imbalance, particularly when hypokalemia or hypomagnesemia occurs, both of which can contribute to inner ear dysfunction.
hypocalcaemia-The loop of Henle is involved in the reabsorption of calcium. By inhibiting the Na+/K+/2Cl- cotransporter, loop diuretics decrease the electrochemical gradient necessary for calcium reabsorption.
renal impairment (from dehydration + direct toxic effect)-Dehydration is a common consequence of diuresis, and if excessive fluid loss occurs without adequate fluid replacement, it can lead to renal hypoperfusion (reduced blood flow to the kidneys) and acute kidney injury (AKI).
Why it happens: Loop diuretics can cause a drop in renal perfusion due to the volume depletion they induce. Additionally, direct nephrotoxic effects may result from high concentrations of the drug or its metabolites in the kidneys, leading to renal dysfunction.
hyperglycaemia (less common than with thiazides)-Loop diuretics can impair insulin secretion and insulin sensitivity. The exact mechanism isn't fully understood, but it's thought to involve alterations in potassium and magnesium balance, which can impact glucose metabolism.
gout-Loop diuretics can cause hyperuricaemia (elevated uric acid levels) by reducing the renal clearance of uric acid. This occurs because diuretics lead to dehydration and a decreased glomerular filtration rate (GFR), which reduces the kidney's ability to excrete uric acid.
109
Which of the drug is contraindicated in VT?
Verapamil
110
anticoagulation after AF what type of anticoagulant is preferred if has a history of valvular heart disease?
warfarin is still preferred to a direct oral anticoagulant.
111
When is a pansystolic murmur heard?
Tricuspid regurgitation
112
What are the signs of tricuspid regurgitation?
Signs
pan-systolic murmur
prominent/giant V waves in JVP
pulsatile hepatomegaly
left parasternal heave
113
114
What are the causes of tricuspid regurgitation?
Causes
right ventricular infarction
pulmonary hypertension e.g. COPD
rheumatic heart disease
infective endocarditis (especially intravenous drug users)
Ebstein's anomaly
carcinoid syndrome
115
What is the diagnostic criteria for infective endocarditis?
Infective endocarditis diagnosed if
pathological criteria positive, or
2 major criteria, or
1 major and 3 minor criteria, or
5 minor criteria
116
What is the pathological criteria for infective endocarditis?
Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)
117
What is the major and minor criteria for infective endocarditis?
Major criteria
Positive blood cultures
two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or
persistent bacteraemia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis, or
positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci, or
positive molecular assays for specific gene targets
Evidence of endocardial involvement
positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or
new valvular regurgitation
Minor criteria
predisposing heart condition or intravenous drug use
microbiological evidence does not meet major criteria
fever > 38ºC
vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots
118
What does Posterior MI typically present on ECG with?
Tall R waves in V1-2
119
What ECG changes are considered normal variants in an athlete?
sinus bradycardia
junctional rhythm
first degree heart block
Mobitz type 1 (Wenckebach phenomenon)
120
What is the drug management for chronic heart failure?
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
adults usually require just one dose but those with asplenia, splenic dysfunction or chronic kidney disease need a booster every 5 years
121
After various unsuccessful attempts of restoring normal cardiac rhythm, the team decides to administer him a drug. After the administration, he complains of severe chest pain, which is self-limiting and terminates quickly.
What drug has this patient been given?
Adenosine-This drug is used to terminate supraventricular tachycardias after vagal manoeuvers have failed. It can cause a brief sensation of flushing and intense chest pain, but the side-effects should resolve fastly. This medication should not be administered to asthmatics as it can cause bronchospasm.
122
What are the adverse affects of amiodarone?
Amiodarone is used in the pharmacological cardioversion of atrial fibrillation. It can cause thyroid dysfunction, corneal deposits, pulmonary and liver fibrosis, 'slate-grey' appearance, and bradycardia but it has not been shown to cause chest pain.
123
What are the adverse affects of Atropine?
Atropine is used in the management of severe bradycardia. It can cause visual sensitivity to light, blurred vision, dry eyes, dry mouth, constipation, and decreased sweating but it has not been shown to cause chest pain.
124
What is Brugada syndrome?
Brugada syndrome is a form of inherited cardiovascular disease that causes an irregular heartbeat with may present with sudden cardiac death.
125
Is brugada syndrome inherited in a dominant or recessive fashion?
dominant
126
What are the ecg changes in brugada syndrome?
ECG changes
convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
partial right bundle branch block
the ECG changes may be more apparent following the administration of flecainide or ajmaline - this is the investigation of choice in suspected cases of Brugada syndrome
127
What is the management of brugada syndrome?
implantable cardioverter-defibrillator
128
What is nicorandil?
Nicorandil is a vasodilatory drug used to treat angina. It is a potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.
129
What are the adverse effects and contraindications of nicorandil?
Adverse effects
headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration
Contraindications
left ventricular failure
130
Pacing is required in heart block following what type of MI?
Complete heart block following an inferior MI is NOT an indication for pacing, unlike with an anterior MI
131
What is Kussmauls sign and when is it seen?
132
What are the features of digoxin toxcity on ECG?
ECG features
down-sloping ST depression ('reverse tick', 'scooped out')
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia
133
When should beta blockers be stopped?
Beta-blockers should only be stopped in acute heart failure if the patient has heart rate < 50/min, second or third degree AV block, or shock
134
Digoxin toxicity ECG features
down-sloping ST depression ('reverse tick', 'scooped out')
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia
135
indications for valve replacment surgery
severe valvular incompetence
aortic abscess (often indicated by a lengthening PR interval)
infections resistant to antibiotics/fungal infections
cardiac failure refractory to standard medical treatment
recurrent emboli after antibiotic therapy
136
Which drug reverses the effects of dabigatran?
idarucizumab
137
Dabigatran
oral anticoagulant that works by being a direct thrombin inhibitor.
138
Both carvedilol and bisoprolol have been shown to reduce mortality in stable heart failure. The other beta-blockers have no evidence base to support their use.
139
ECG features may be seen in hypokalaemia:
small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT
140
