MED: Cardiology Flashcards
RFs for ACS?
Unmodifiable:
- Increasing age
- Male
- FHx
Modifiable:
- Smoking
- Diabetes
- Hypercholesterolaemia
- Hypertension
- Obesity
What is ischaemic heart disease?
= Coronary heart disease / coronary artery disease
The gradual build up of fatty plaques within the walls of the coronary arteries. This leads to two main problems:
- 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
- The risk of sudden plaque rupture. The fatty plaques which have built up in the endothelium may rupture leading to sudden occlusion of the artery. This can result in no blood/oxygen reaching the area of myocardium.
What ECG changes are seen during acute MI?
- Hyperacute T waves often first sign of MI but often only persists for a few minutes
- ST elevation may then develop
- T wave inversion typically within first 24 hours. Can last days to months
- Pathological Q waves develop after several hours to days - usually persists indefinitely
What criteria is needed to diagnose a STEMI?
Clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration)
AND
Persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
- 2.5mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men <40yrs, or ≥2.0mm ST elevation in leads V2-3 in men >40yrs
- 1.5mm ST elevation in V2-3 in women
- 1mm ST elevation in other leads
- New LBBB (LBBB should be considered new unless there is evidence otherwise)
ECG changes in leads V1-4 correlate to which territory and artery?
Anteroseptal
LAD
ECG changes in leads II, II, aVF correlate to which territory and artery?
Inferior
Right coronary
ECG changes in leads V4-6, I, aVL correlate to which territory and artery?
Anterolateral
LAD or left circumflex
ECG changes in leads I, aVL +/- V5-6 correlate to which territory and artery?
Lateral
Left circumflex
Tall R waves in V1-2 correlate to which territory and artery?
Posterior
Usually left circumflex
Also right coronary
Describe the common management of all patients with ACS
- Aspirin 300mg
- Oxygen if patient has sats <94%
- Morphine if severe pain
- Nitrates - sublingually or IV - useful if ongoing chest pain or hypertension (used in caution if patient hypotensive)
What are the 2 types of coronary reperfusion therapy?
Primary coronary intervention:
- Offered if presentation is within 12 hours of onset of symptoms AND PCI can be delivered within 2 hours of the time when thrombolysis could have been given (i.e. consider thrombolysis if there is a significant delay in being able to provide PCI)
- If patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered
- Drug-eluting stents are now used
- Radial access is preferred to femoral access
Thrombolysis:
- Should be offered within 12 hours of onset of symptoms if primary PCI cannot be delivered within 2 hours of the time when thrombolysis could have been given
- If the patient’s ECG taken 90 minutes after thrombolysis failed to show resolution of the ST elevation then they would then require transfer for PCI
Describe the management of STEMI with PCI
Further antiplatelet prior to PCI:
// ‘dual antiplatelet therapy’
- If patient not taking an oral anticoagulant: prasugrel
- If taking oral anticoagulant: clopidogrel
Drug therapy during PCI:
- Radial access = Unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI)
- Femoral access = Bivalirudin with bailout GPI
Other procedures during PCI:
- Thrombus aspiration, but not mechanical thrombus extraction, should be considered
- Complete revascularisation should be considered for patients with multivessel coronary artery disease without cardiogenic shock
What further drug therapy is used for NSTEMI/unstable?
Antithrombin treatment:
- Fondaparinux offered to patients not at high risk of bleeding and not having angiography immediately
- If immediate angiography planned or a patients creatinine is >265µmol/L then unfractionated heparin should be given
What tool is used for risk assessment for ACS?
The Global Registry of Acute Coronary Events (GRACE)
What factors does the GRACE score take into account?
- age
- heart rate, blood pressure
- cardiac (Killip class) and renal function (serum creatinine)
- cardiac arrest on presentation
- ECG findings
- troponin levels
Which patients with NSTEMI/unstable angina should have a coronary angiography (with follow-on PCI if necessary)?
Immediate:
- Patients who are clinically unstable (e.g. hypotensive)
Within 72 hours:
- Patients with a GRACE score > 3% i.e. those at immediate, high or highest risk
Coronary angiography should also be considered for patients if ischaemia is subsequently experienced after admission
Describe the management of NSTEMI with PCI
Further drug therapy:
- Unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not
- Further antiplatelet (‘dual antiplatelet therapy’, i.e. aspirin + another drug) prior to PCI
-If the patient is not taking an oral anticoagulant: prasugrel or ticagrelor
-If taking an oral anticoagulant: clopidogrel
Describe the conservative management of NSTEMI/unstable
Further drug therapy:
- Further antiplatelet (‘dual antiplatelet therapy’, i.e. aspirin + another drug)
- If the patient is not at a high-risk of bleeding: ticagrelor
- If the patient is at a high-risk of bleeding: clopidogrel
What are some complications of MI?
Cardiac arrest:
- Most commonly occurs due to patients developing VF and is most common cause of death following a MI
- Managed as per ALS protocol with defibrillation.
Cardiogenic shock:
- Patients may require inotropic support and/or an intra-aortic balloon pump.
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
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.
- Characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR
- Treated with NSAIDs.
Left Ventricular Aneurysm:
- 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:
- Occurs around 1-2 weeks afterwards.
- Patients present with acute heart failure secondary to cardiac tamponade
- Urgent pericardiocentesis and thoracotomy are required.
VSD:
- 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.
What system is used to stratify risk post myocardial infarction?
Killip class
What are the 2 types of acute heart failure?
De novo AHF:
- Ischaemia
- Viral myopathy
- Toxins
- Valve dysfunction
Decompensated AHF:
- Acute coronary syndrome
- Hypertensive crisis: e.g. bilateral renal artery stenosis
- Acute arrhythmia
- Valvular disease
What are the clinical features of AHF?
What are the investigations for AHF?
Bloods:
- To look for any underlying abnormality such as anaemia, abnormal electrolytes or infection.
- B-type natriuretic peptide – raised levels (>100mg/litre) indicate myocardial damage and are supportive of the diagnosis.
Chest X-ray:
- Findings include pulmonary venous congestion, interstitial oedema and cardiomegaly
Echo:
- Will identify pericardial effusion and cardiac tamponade
What is the management of AHF?
- IV loop diuretics
- oxygen
- vasodilators - if myocardial ischaemia, severe hypertension or regurgitant aortic or mitral valve disease
- CPAP if respiratory failure
if severe hypotension / shock:
- inotropic agents e.g. dobutamine
- vasopressor agents e.g. norepinephrine
- mechanical circulatory assistance: e.g. intra-aortic balloon counterpulsation or ventricular assist devices
What are the causes of acute pericarditis?
- viral infections (Coxsackie)
- tuberculosis
- uraemia
- post-myocardial infarction
- early (1-3 days): fibrinous pericarditis
- late (weeks to months): autoimmune pericarditis (Dressler’s syndrome)
- radiotherapy
- connective tissue disease
- systemic lupus erythematosus
- rheumatoid arthritis
- hypothyroidism
- malignancy (lung cancer, breast cancer)
- trauma
What are the clinical features of acute pericarditis?
Retrosternal chest pain: (85-90%)
- Usually sharp and pleuritic in nature
- Improved by sitting up and leaning forward
- Radiation to the trapezius ridge is considered to be specific for pericarditis
Pericardial friction rub: (≤33%)
- Superficial, scratchy or squeaky quality on auscultation, best heard using the diaphragm of the stethoscope
- Usually best heard at the left lower sternal border
- Can be differentiated from pleural rub by asking patient to hold their breath
- Highly specific for pericarditis but has a low sensitivity
Patients may exhibit other clinical features that suggest an infectious aetiology:
- Low-grade fever
- Prodromal myalgia and malaise
What are the investigations for acute pericarditis?
Bedside tests:
ECG
- Widespread concave ST-elevations with PR-segment depression
- PR-segment depression is 85% specific for acute pericarditis, but not sensitive
- T-wave changes may last for weeks after resolution of symptoms but are of no clinical significance
Bloods:
- C-reactive protein, ESR, FBC - can also be used to monitor progress
- Serum troponins
- Urea - elevation suggests uraemic aetiology of the pericarditis
Imaging:
Echo
- Mild pericardial effusion seen in 60% of patients
Chest X-ray
- Often normal unless there is a large pericardial effusion or lung pathology that can be visualised, such as lung malignancy
- New or unexplained cardiomegaly may also suggest acute pericarditis
Further imaging (CT and MRI) considered in unclear diagnostic cases to better visualise pericardial inflammation. MRI may also be used to confirm myocardial involvement
Pericardiocentesis only indicated when suspicion of bacterial or neoplastic aetiology. It may also be done as a therapeutic intervention for a large pericardial effusion.
Other investigations can be considered if a specific cause is suspected, but are not routine
- Blood cultures if fever >38ºC, signs of sepsis or concomitant bacterial infection elsewhere
- HIV serology
- Interferon-gamma release assay or tuberculin skin test
What is the management of acute pericarditis?
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 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
- Combination of NSAIDs and colchicine 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
What are the complications of acute pericarditis?
Recurrent pericarditis (15-30%):
- Recurrence after a symptom-free interval of 4-6 weeks
- Recurrence rate increased to 50% in patients not treated with colchicine
Acute cardiac tamponade:
- More common in patients with underlying malignancy, TB or purulent pericarditis
- Treated by pericardiocentesis
Chronic constrictive pericarditis:
- More common in patients with TB or purulent pericarditis or immune-mediated and neoplastic aetiologies
- Treated by surgical pericardial resection
How do NICE define anginal pain?
- Constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
- Precipitated by physical exertion
- Relieved by rest or GTN in about 5 minutes
Interpretation:
- 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
What are the investigations for angina if it cannot be concluded clinically?
1st line: CT coronary angiography
2nd line: Non-invasive functional imaging (looking for reversible myocardial ischaemia)
3rd line: Invasive coronary angiography
Examples of non-invasive functional imaging:
- Myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or
- Stress echocardiography or
- First-pass contrast-enhanced magnetic resonance (MR) perfusion or
- MR imaging for stress-induced wall motion abnormalities
Describe the management of stable angina
- All patients should receive aspirin and a statin
- Sublingual GTN to abort angina attacks
- Beta-blocker or a CCB first-line for prevention
- If CCB monotherapy = rate-limiting one e.g. verapamil or diltiazem
- If CCB combination with beta-blocker = long-acting CCB (e.g. amlodipine, modified-release nifedipine).
- Beta-blockers should not be prescribed with verapamil (risk of complete heart block)
- Second line = medication increased to maximum tolerated dose (e.g. for atenolol 100mg od)
- Third line = combination therapy (beta-blocker and CCB)
- If a patient is on monotherapy and cannot tolerate the addition of a CCB or a beta-blocker then consider one of the following drugs: a long-acting nitrate, ivabradine, nicorandil or ranolazine
Describe nitrate tolerance
Many patients who take nitrates develop tolerance and experience reduced efficacy
- The BNF advises that patients who develop tolerance should take the second dose of isosorbide mononitrate after 8 hours, rather than after 12 hours. This allows blood-nitrate levels to fall for 4 hours and maintains effectiveness
- This effect is not seen in patients who take modified-release isosorbide mononitrate
What is aortic dissection?
Aortic dissection is a severe, life-threatening condition characterized by the separation of the aortic wall layers, resulting in the formation of a false lumen.
What are the causes of aortic dissection?
- 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
Describe the classification of aortic dissection
Stanford classification:
- type A - ascending aorta, 2/3 of cases
- type B - descending aorta, distal to left subclavian origin, 1/3 of cases
DeBakey classification:
- type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
- type II - originates in and is confined to the ascending aorta
- type III - originates in descending aorta, rarely extends proximally but will extend distally
What are the clinical features of aortic dissection?
- chest pain: typically severe, radiates through to the back and ‘tearing’ in nature
- 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
What are the investigations for aortic dissection?
Chest x-ray:
- widened mediastinum
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
Transoesophageal echocardiography (TOE):
- more suitable for unstable patients who are too risky to take to CT scanner
What is the management of aortic dissection?
Type A:
- surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention
Type B:
- conservative management
- bed rest
- reduce blood pressure IV labetalol to prevent progression
What are the causes of aortic stenosis?
Congenital valvular AS:
- In children, unicuspid aortic valve is the most common cause of symptomatic AS (William syndrome is a RF for supravalvular AS)
- In adults, bicuspid aortic valve can lead to AS in people at an earlier age than those who acquire AS
The valve is at an increased risk of calcification and degeneration
Acquired valvular AS:
- Initially thought to be a ‘wear-and-tear’ process due to aging, data now suggests that atherosclerosis plays a role in causing the aortic valve to have endothelial dysfunction and then progress to calcification.
- In those aged over 65 years, the frequency of AS is 4-5%
- RFs include hypertension, diabetes mellitus, hypercholesterolaemia, smoking (similar to atherosclerosis)
- Aortic sclerosis: thickening and calcification of the orifice without a pressure gradient - Progresses to AS at a rate of 1.8-1.9% per year
- Rheumatic heart disease can cause fibrosis of the valve leaflets leading to commissural fusion.
What are the clinical features of aortic stenosis?
> May be asymptomatic for a prolonged period of 10-20 years
Common symptoms:
- Exertional dyspnoea
- May have reduced exercise tolerance and fatigability
- Exertional angina
- Exertional syncope or presyncope
They may have heart failure (HF) with end-stage disease due to left ventricular outflow obstruction:
- This may present with paroxysmal nocturnal dyspnea, orthopnoea, dyspnea on exertion, bilateral lower limb oedema and/or pulmonary oedema.
Also:
- AF also common in patients with HF from AS
- Moreover, patients may present with gastrointestinal bleeding due to angiodysplasia (Heyde’s syndrome)
What are the signs of aortic stenosis on cardiac examination?
Loud mid-to-late peaking systolic ejection murmur
- Early peaking is more consistent with mild or moderate AS and late peaking is consistent with severe AS
- Murmur radiates to the carotids and becomes more prominent with sitting forward and in expiration
- Murmur becomes softer the more severe the stenosis
- May also radiate to the apex and have a musical quality (gallavardin phenomenon); not to be confused with mitral regurgitation
With severe AS they may also have:
- Slow-rising and low volume carotid pulse (pulsus parvus et tardus) (May not be present in elderly due to stiff vascular vessels)
- Soft or absent second heart sound (S2)
- Narrow pulse pressure
- Reverse splitting of S2
- Heaving apex beat or systolic thrill
- Signs of heart failure - pitting lower limb oedema, bilateral basal crackles
- S4
What are the investigations for aortic stenosis?
Initial work-up:
ECG: may show arrhythmias or signs of left ventricular (LV) strain
- LV hypertrophy is present in about 80% of severe AS patients
- Atrial fibrillation or coronary artery disease (CAD) can also be detected
Chest X-ray:
Transthoracic echocardiogram (TTE): the diagnosis of AS is established by TTE.
- It helps to calculate the trans-valvular velocity, mean pressure gradient, and aortic valve area which helps determine the extent of the stenosis.
- It also helps asses left ventricular function, flow status, and wall thickness.
Additional tests for prognostic information:
- Exercise stress testing (EST): useful to unmask symptoms in physically active patients if they are asymptomatic or have non-specific symptoms with severe AS
- Dobutamine stress echocardiogram: useful for patients who have low-gradient AS
- Patients may be symptomatic but have seemingly low pressures due to a low ejection fraction
- Gradient will increase > 40 mmHg after administration of low dose dobutamine
- B-type natriuretic peptide (BNP): assess for heart failure, predict the timing of intervention for asymptomatic patients and symptom-free survival in severe AS
- Multi-slice computed tomography (MSCT): extent of calcification to determine calcium score for severity of AS and may be used to detect CAD in patients who are not eligible for EST
- Cardiac magnetic resonance: quantify myocardial fibrosis
- Cardiac catheterization: for a definitive diagnosis if noninvasive testing is non-diagnostic however it is not routinely done.
What investigations need to be done prior to surgical aortic valve replacement (SAVR) or transcatheter aortic valve implantation (TAVI)?
Coronary angiogram:
- To identify co-existing CAD and conduct concomitant coronary revascularization if possible
- Pertinent in patients who have cardiovascular risk factors, prior cardiovascular disease, suspected myocardial ischemia, left ventricular dysfunction, are men > 40 years or post-menopausal women
Trans-oesophageal echocardiogram (TOE): to assess for endocarditis and mitral valve abnormalities as well as monitoring the TAVI procedure
MSCT: assess the anatomy and dimensions of the aortic root, shape of the aortic valve annulus and the number of aortic valve cusps
What is the management of aortic stenosis?
Indication for surgical treatment:
- Symptomatic
- Severe AS: classified as aortic jet velocity ≥4 m/s, mean trans-valvular pressure gradient ≥ 40 mmHg, and aortic valve area ≤1 cm2 - Surgery should be performed promptly after symptom onset. If symptoms are not elicited by history, they should undergo exercise stress testing (~30% of patients will become symptomatic) - Also indicated if asymptomatic but have the following - left ventricular ejection fraction (LVEF) <50%, undergoing other cardiac surgery, a low surgical risk with risk factors or low exercise tolerance
Choice between TAVI and SAVR:
Made by weighing individual patient factors against the risks of providing each modality.
- Risk stratification may be carried out using scoring systems like euroSCORE, society of thoracic surgeons (STS), etc. For example, if the euroSCORE/STS score is <4% and patients have co-morbidities, SAVR is preferred.
- According to NICE guidelines, sutureless aortic valve replacement (SUAVR) is an effective alternative treatment to SAVR or TAVI as it may be a quicker procedure and allows for both coronary arteries and valve to be treated concurrently.
Percutaneous balloon valvotomy is used as a palliative measure for patients that may not be suitable for cardiac surgery or are critically ill. It is also used in children and young adults with congenital AS.
Conservative management is indicated for patients with mild AS who are asymptomatic and have no risk factors
- This may include treating heart failure, maintaining sinus rhythm, and controlling hypertension with regular follow-up.
- Serial testing should be done every 6 months for asymptomatic severe AS and yearly for mild-to-moderate AS.
- Surgery may be considered if predictive factors of adverse outcomes and symptom development such as elevated BNP, older age, cardiovascular risk factors and extremely abnormal echocardiographic parameters are present.
What are some RFs for AF?
- Hypertension
- Ischaemic Heart Disease
- Heart Failure, including due to valvular disease
- Cardiomyopathy
- Cardiothoracic surgery
- Diabetes Mellitus
- Obesity
- Pneumonia
- Smoking
- Obstructive Sleep Apnoea
- Thyrotoxicosis
- Caffeine
- Alcohol excess
- Chronic kidney disease
- Increasing age
- Male
Describe the classification of AF
Acute (<48 hours)
Paroxysmal (self-limiting, <7 days, recurs)
Persistent (>7 days, may recur even after cardioversion)
Describe the clinical features of AF
Asymptomatic
Non-life threatening:
- Palpitations
- Fatigue
Complications:
- Ischaemic stroke
- Mesenteric ischaemia
- Acute limb ischaemia
Haemodynamic instability:
- Acute heart failure - SOB (pulmonary oedema), raised JVP
- Cardiogenic shock - tachycardia >150, hypotension <90, syncope or pre-syncope / dizziness
- Cardiac chest pain, including MI - most common in patients with some level of pre-existing coronary heart disease
What are the investigations for AF?
Assessment of the radial pulse:
- irregularly irregular
- must be followed up with an immediate ECG to confirm the diagnosis
ECG monitoring:
- irregularly irregular QRS complexes with a fibrillating baseline devoid of p-waves
Long term electrical recordings e.g. 24 hour ECGs / event recorders:
- can be used to confirm AF in patients who remain without a diagnosis following normal ECG recordings - most commonly in patients with paroxysmal AF who receive ECG recordings between episodes
To investigate underlying cause:
- Bloods - FBC, U&Es, LFTs, TFTs, Ca and Mg, Blood glucose (finger prick and blood)
- Transthoracic echo
- CXR
For how long before and after cardioversion for arrhythmia should a patient be anti-coagulated?
3w before and 4w after OR lifelong (if CHA2DS2VASc high or if paroxysmal AF)
How can chadsvasc score be used to determine the need for longterm anticoagulation?
Score:
0 = no need for longterm anticoagulation
1 = anticoagulate if male, do not anticoagulate if female
2 or more: anticoagulate
What is the main contraindication to be aware of for all CCBs?
Peripheral oedema
What are the 1st, 2nd and 3rd line options for rate control in AF?
1st line: beta blocker or CCB (verapamil is better than dilitiazem)
2nd line: combination therapy with any 2 of the following:
betablocker
diltiazem
digoxin
With what waveform on the ECG should DC cardioversion be synchronised?
R wave
If synchronised with T wave it can cause VT
Describe the methods of rhythm control
- DC Cardioversion - use of electrical stimulation to restore sinus rhythm
- Chemical cardioversion - Amiodarone (suitable in most patients), flecainide (contraindicated in structural or ischaemic heart disease)
Recall 2 surgical options for managing AF
Radiofrequency ablation of AV node
Maze procedure
Describe rhythm control for AF <48hrs
- Patients should be heparinised
- Cardioverted with electrical or chemical
- Further anticoagulation is unnecessary
Describe rhythm control for AF >48hrs
- Anticoagulation should be given for at least 3 weeks prior to cardioversion
- An alternative strategy is to perform a 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
- Following electrical cardioversion, patients should be anticoagulated for at least 4 weeks.
Recall the components of the CHA2DS2VASc score
CHF
HTN
Age >75
DM
Stroke
Vascular disease
Age 65-74
Sex Category (female)
Describe the anticoagulation used in AF
First line = DOACs:
- Oral anticoagulants including Rivaroxaban, Apixaban and Dabigatran
Second line = Warfarin:
- INR of 2-3 for most patients without valve disease
- Prescribed with LMWH until its anticoagulant effect is established, as it is initially prothrombotic
Within what window of AF beginning can it be treated differently to longer-standing AF? What is this different treatment?
AF <48 hours duration and HAEMODYNAMICALLY UNSTABLE can be cardioverted electrically
Difficult to establish onset of AF as patient may not have palpitations, or may be unsure as to when they started
For how long before and after cardioversion for arrhythmia should a patient be anti-coagulated?
3w before and 4w after OR lifelong (if CHA2DS2VASc high or if paroxysmal AF)
What is atrial flutter?
A supraventricular tachyarrhythmia characterized by rapid and regular atrial depolarizations typically occurring at a rate of 250-350 beats per minute
What are the clinical features of atrial flutter?
- Sx associated with haemodynamic compromise such as dyspnea, fatigue, lightheadedness, presyncope or syncope
- Palpitations - abrupt onset and termination of palpitations along with an awareness of rapid or irregular heartbeats
- Chest pain
- Worsening heart failure symptoms such as orthopnea, paroxysmal nocturnal dyspnea, and peripheral oedema
- Individuals are at risk for systemic embolization manifesting as TIAs or cerebrovascular accidents
On examination
- Irregularly irregular pulse
- Auscultation of the heart may reveal a “saw-tooth” pattern in the jugular venous waveform and varying intensity of the first heart sound (S1).
- Additionally, signs of congestive heart failure such as pulmonary rales or peripheral oedema may be present.
What is cardiac tamponade?
Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure
What are the clinical features of cardiac tamponade?
Classical features - Beck’s triad:
- Hypotension
- Raised JVP
- Muffled heart sounds
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
Describe the classification of CHF
NYHA Class I:
- No symptoms
- No limitation
NYHA Class II:
- Mild symptoms
- Slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea
NYHA Class III:
- Moderate symptoms
- Marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms
NYHA Class IV:
- Severe symptoms
- Unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity
What are the clinical features of CHF?
- dyspnoea
- cough: may be worse at night and associated with pink/frothy sputum
- orthopnoea
- paroxysmal nocturnal dyspnoea
- wheeze (‘cardiac wheeze’)
- weight loss (‘cardiac cachexia’): occurs in up to 15% of patients. Remember this may be hidden by weight gained secondary to oedema
- bibasal crackles on examination
- ankle oedema
What are the investigations for CHF?
> > All patients should have an NT‑proBNP blood test first-line.
- If levels are ‘high’ (>2000) arrange specialist assessment (including transthoracic echocardiography) within 2 weeks
- If levels are ‘raised’ (400-2000) arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks
Describe the management of CHF
*First-line = BB and ACE-I**
- Generally, one drug should be started at a time
- No effect on mortality in heart failure with preserved EF
Second-line = Aldosterone antagonist
- E.g. spironolactone and eplerenone
SGLT-2 inhibitors:
- HF with reduced EF
- add-on to optimised standard care
Third line:
- Ivabradine - criteria = sinus rhythm >75/min and a left ventricular fraction <35%
- Sacubitril-valsartan - criteria = left ventricular fraction < 35%, initiated following ACEi or ARB wash-out period
- Hydralazine in combination with nitrate - particularly indicated in Afro-Caribbean patients
- Digoxin - strongly indicated if there is coexistent AF
- Cardiac resynchronisation therapy - indications = widened QRS (e.g. LBBB) complex
Also:
- Diuretics should be given for fluid overload
- Offer annual influenza vaccine
- Offer one-off pneumococcal vaccine
What must be monitored whilst patients are on spironolactone?
Potassium (as is a potassium-sparing diuretic)
Recall some drugs that are contra-indicated in heart failure
Thiozolidinediones (type 2 diabetes)
Verapamil (as is negative inotrope)
NSAIDs (can cause fluid retention)
Glucocorticoids (can cause fluid retention)
Flecainide (negative inotrope, arrhythmogenic)
What are the risk factors for a DVT?
- Male, over 60
- Immobilisation: hospitalisation, bedbound, long haul flights
- Inflammatory state: vasculitis, sepsis
- Malignancy - patients who have an unprovoked DVT need a thorough history and examination to screen for malignancy
- Medication: chemotherapy, hormone replacement therapy/oral contraceptive pill
- Obesity
- Pregnancy
- Previous venous thromboembolism (may indicate underlying thrombophilia)
- Recent surgery or trauma
- Smoking
- Varicose veins
Describe the WELLS score
Clinical probability simplified score:
DVT likely: 2 points or more
DVT unlikely: 1 point or less
What are the investigations for a DVT?
DVT ‘likely’ (2 points or more):
- Proximal leg vein ultrasound scan within 4 hours
- Positive = DVT > start anticoagulant treatment
- Negative > D-dimer test
- Negative scan and negative D-dimer = diagnosis unlikely > alternative diagnoses should be considered
- If proximal leg vein ultrasound scan cannot be carried out within 4 hours > D-dimer test and interim therapeutic anticoagulation administered whilst waiting for the proximal leg vein ultrasound scan (which should be performed within 24 hours)
- Interim therapeutic anticoagulation = DOAC such as apixaban or rivaroxaban
- If scan is negative but D-dimer is positive = stop interim therapeutic anticoagulation and offer repeat proximal leg vein ultrasound scan 6 to 8 days later
DVT ‘unlikely’ (1 point or less):
- D-dimer test within 4 hours
- If not, interim therapeutic anticoagulation given until result available
- Negative = DVT unlikely and alternative diagnoses should be considered
- Positive = proximal leg vein ultrasound scan within 4 hours
- If scan cannot be carried out within 4 hours interim therapeutic anticoagulation should be administered whilst waiting (which should be performed within 24 hours)
What is the management of a DVT?
- DOAC - apixaban or rivaroxaban should be offered first-line following the diagnosis of a DVT
- 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 use a DOAC, unless contraindicated
- 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
What length of anticoagulation is required following a DVT?
ALL patients should have anticoagulation for at least 3 months
- A provoked VTE // due to an obvious precipitating event e.g. immobilisation following major surgery = 3m (3 to 6 months for people with active cancer)
- An unprovoked VTE occurs = 6m
Describe post-thrombotic syndrome
Venous outflow obstruction and venous insufficiency result in chronic venous hypertension. The resulting clinical syndrome is known as post-thrombotic syndrome
- painful, heavy calves
- pruritus
- swelling
- varicose veins
- venous ulceration
Management = Compression stockings + leg elevation
What are the causes of HTN?
Primary / Essential:
- Age, family history, obesity, high salt intake, sedentary lifestyle, and alcohol consumption
Secondary:
- RENAL - Glomerulonephritis, chronic pyelonephritis, adult PKD, renal artery stenosis
- ENDO - Primary hyperaldosteronism, phaeochromocytoma, Cushing’s syndrome, Congenital adrenal hyperplasia, Acromegaly
- Glucocorticoids
- NSAIDs
- Pregnancy
- Coarctation of the aorta
- COCP
Describe the medical management of HTN
What should the target BP be?
Describe the management of changes in INR
First degree heart block ?
- PR interval > 0.2 seconds
- Asymptomatic first-degree heart block is relatively common and does not need treatment
Second degree heart block Type 1?
Type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs
Second degree heart block Type 2?
Type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex
Third degree heart block ?
No association between the P waves and QRS complexes
