Cardiology Flashcards
What is the cut off blood pressure value for further investigation
Age < 80 years
Clinic 140/90 mmHg ABPM 135/85 mmHg
Age > 80 years
Clinic150/90 mmHg ABPM 145/85 mmHg
What is offered if BP is found to be over 140/90
Ambulatory BP monitoring or home BP monitoring
What is done if on ABPM or HBPM BP remains below 135/85
nothing
What is stage 1 hypertension? When is this treated?
Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
Treat if <80 years and any of the following
-target organ damage
-established cardiovascular disease
-renal disease
-diabetes
-10 yr cardiovascular risk greater than or equal to 10%
What is stage 2 hypertension? when is this treated?
Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
-treat all
What is severe hypertension?
Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg
When would you admit for specialist assessment of severe hypertension?
admit for specialist assessment if:
signs of retinal haemorrhage or papilloedema (accelerated hypertension) or life-threatening symptoms such as new-onset confusion, chest pain, signs of heart failure, or acute kidney injury
NICE also recommend referral if a phaeochromocytoma is suspected (labile or postural hypotension, headache, palpitations, pallor and diaphoresis)
What is done for severe hypertension that doesn’t warrant admission?
if none of the above then arrange urgent investigations for end-organ damage (e.g. bloods, urine ACR, ECG)
if target organ damage is identified, consider starting antihypertensive drug treatment immediately, without waiting for the results of ABPM or HBPM. if no target organ damage is identified, repeat clinic blood pressure measurement within 7 days
What is ABPM? and what is offered if this isnt tolerated or declined?
Ambulatory blood pressure monitoring (ABPM)
at least 2 measurements per hour during the person's usual waking hours (for example, between 08:00 and 22:00) use the average value of at least 14 measurements
If ABPM is not tolerated or declined HBPM should be offered
What is HBPM?
Home blood pressure monitoring (HBPM)
for each BP recording, two consecutive measurements need to be taken, at least 1 minute apart and with the person seated BP should be recorded twice daily, ideally in the morning and evening BP should be recorded for at least 4 days, ideally for 7 days discard the measurements taken on the first day and use the average value of all the remaining measurements
Describe lifestyle modifications that should be advised for patients to lower BP
a low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. The average adult in the UK consumes around 8-12g/day of salt. A recent BMJ paper* showed that lowering salt intake can have a significant effect on blood pressure. For example, reducing salt intake by 6g/day can lower systolic blood pressure by 10mmHg
caffeine intake should be reduced
the other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich in fruit and vegetables, exercise more, lose weight
Descrbe stage 1 management of hypertension
patients < 55-years-old or a background of type 2 diabetes mellitus: ACE inhibitor or a Angiotensin receptor blocker (ACE-i or ARB): (A)
angiotensin receptor blockers should be used where ACE inhibitors are not tolerated (e.g. due to a cough)
patients >= 55-years-old or of black African or African–Caribbean origin: Calcium channel blocker (C)
ACE inhibitors have reduced efficacy in patients of black African or African–Caribbean origin are therefore not used first-line
Describe stage 2 management of hypertension
if already taking an ACE-i or ARB add a Calcium channel blocker or a thiazide-like Diuretic
if already taking a Calcium channel blocker add an ACE-i or ARB or a thiazide-like Diuretic
for patients of black African or African–Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor
(A + C) or (A + D) or (C + A) or (C + D)
Describe stage 3 treatment of hypertension
add a third drug to make, i.e.:
if already taking an (A + C) then add a D
if already (A + D) then add a C
(A + C + D)
Describe stage 4 treatment of hypertension
NICE define step 4 as resistant hypertension and suggest either adding a 4th drug (as below) or seeking specialist advice
first, check for:
confirm elevated clinic BP with ABPM or HBPM
assess for postural hypotension.
discuss adherence
if potassium < 4.5 mmol/l add low-dose spironolactone
if potassium > 4.5 mmol/l add an alpha- or beta-blocker
What is the most common cause of secondary hypertension?
primary hyperaldosteronism, including Conn’s syndrome. This makes it the single most common cause of secondary hypertension.
What are 4 renal causes of secondary hypertension?
Renal disease accounts for a large percentage of the other cases of secondary hypertension. Conditions which may increase the blood pressure include:
glomerulonephritis pyelonephritis adult polycystic kidney disease renal artery stenosis
What are 5 endocrine causes of secondary hypertension?
Endocrine disorders (other than primary hyperaldosteronism) may also result in increased blood pressure:
phaeochromocytoma Cushing's syndrome Liddle's syndrome congenital adrenal hyperplasia (11-beta hydroxylase deficiency) acromegaly
What are 5 drug causes of hypertension?
Drug causes:
steroids
monoamine oxidase inhibitors
the combined oral contraceptive pill
NSAIDs
leflunomide
What are the blood pressure targets for patients with T1DM? What drug is first line? what drug should be avoided?
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
Because ACE inhibitors/or angiotensin-II receptor antagonist (A2RBs) have a renoprotective effect in diabetes they are the first-line antihypertensive regardless of age.
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.
What is BNP? What are 3 causes of raised BNP? What are 3 causes of reduced BNP?
B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain.
Whilst heart failure is the most obvious cause of raised BNP levels any cause of left ventricular dysfunction such as myocardial ischaemia or valvular disease may raise levels. Raised levels may also be seen due to reduced excretion in patients with chronic kidney disease. Factors which reduce BNP levels include treatment with ACE inhibitors, angiotensin-2 receptor blockers and diuretics.
What are three effects of BNP?
Effects of BNP
vasodilator diuretic and natriuretic suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
What are four clinical uses of BNP?
Diagnosing patients with acute dyspnoea
-a low concentration of BNP(< 100pg/ml) makes a diagnosis of heart failure unlikely, but raised levels should prompt further investigation to confirm the diagnosis
-NICE currently recommends BNP as a helpful test to rule out a diagnosis of heart failure
Prognosis in patients with chronic heart failure
-initial evidence suggests BNP is an extremely useful marker of prognosis
Guiding treatment in patients with chronic heart failure
-effective treatment lowers BNP levels
Screening for cardiac dysfunction
-not currently recommended for population screening
What is the mechanism of action of ACE inhibitors?
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
renoprotective mechanism
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
What are the 4 common 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
What are the 5 cautions/contraindications of ACEI
-pregnancy and breastfeeding - avoid
-renovascular disease - may result in renal impairment
-aortic stenosis - may result in hypotension
-hereditary of idiopathic angioedema
-specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L
What is the interaction between diuretics and ACEI?
patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day)
significantly increases the risk of hypotension
Describe the monitoring of ACEI
urea and electrolytes should be checked before treatment is initiated and after increasing the dose
a rise in the creatinine and potassium may be expected after starting ACE inhibitors
acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l.
significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis
When are ARBs used? who should you exercise caution in? what is the mechanism?
Given to patients who can’t tolerate ACEI (usually due to cough)
Like ACE inhibitors they should be used with caution in patients with renovascular disease. Side-effects include hypotension and hyperkalaemia.
Mechanism - block effects of angiotensin II at the AT1 receptor
What is the treatment of all patients who present with an ACS?
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
What are the ECG criteria for patients with STEMI?
STEMI criteria
clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
1.5 mm ST elevation in V2-3 in women
1 mm ST elevation in other leads
new LBBB (LBBB should be considered new unless there is evidence otherwise)
When is PCI offered? what kind of stents are used? what access is preferred?
percutaneous coronary intervention
should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis 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. Previously 'bare-metal' stents were sometimes used but have higher rates of restenosis radial access is preferred to femoral access
When is fibrinolysis offered?
fibrinolysis
should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given a practical example may be a patient who presents with a STEMI to a small district general hospital (DGH) that does not have facilities for PCI. If they cannot be transferred to a larger hospital for PCI within 120 minutes then fibrinolysis should be given. If the patient's ECG taken 90 minutes after fibrinolysis failed to show resolution of the ST elevation then they would then require transfer for PCI
what antiplatelets are given prior to PCI?
Further antiplatelet prior to PCI
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
What drug therapy is given 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
What procedures other than stenting can be done during PCI?
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
Describe the management of patients with NSTEMI/unstable angina
- Aspirin 300mg and fondaparinux (if PCI not planned immediately)
- Estimate a 6 month mortality (GRACE)
- if low risk <=3% give ticagrelor
-If high risk >3% do PCI, offer immediately or within 72hrs. Add prasugrel or ticagrelor, give unfractionated heparin, use drug-eluting stents
How does the management of patients with NSTEMI/unstable angina change if they are at high risk of bleeding?
Consider swapping fondaparinux to a different antithrombin/dose, swapping prasugrel for ticagrelor or ticagrelor for clopidogrel
If patients on anitcoagulations use clopidogrel
What is the grace score?
-what 6 factors are taken into consideration?
The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It can be calculated using online tools and takes into account the following factors:
age heart rate, blood pressure cardiac (Killip class) and renal function (serum creatinine) cardiac arrest on presentation ECG findings troponin levels
Describe the risk stratification of the GRACE score
Predicted 6mth mortality, risk of future adverse cardiac events
1.5% or below Lowest
> 1.5% to 3.0% Low
> 3.0% to 6.0% Intermediate
> 6.0% to 9.0% High
over 9.0% Highest
Describe the further durg therapy given to patients going for PCI with unstable angina/NSTEMI
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 further drug therapy for patients who are medically managed with NSTEMI/Unstable angina
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 is the mechanism of action of clopidogrel? What is an important interaction?
Mechanism
antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets
Change omeprazole to lansoprazole
Describe chest pain in MI
Cardiac-sounding pain
heavy, central chest pain they may radiate to the neck and left arm nausea, sweating elderly patients and diabetics may experience no pain
Risk factors for cardiovascular disease
What is the diagnosis?
History of asthma, Marfan’s etc
Sudden dyspnoea and pleuritic chest pain
Pneumothorax
Describe the features and risk factors of PE
Sudden dyspnoea and pleuritic chest pain
Calf pain/swelling
Current combined pill user, malignancy
What is the diagnosis?
Sharp pain relieved by sitting forwards
May be pleuritic in nature
Pericarditis
What is pericarditis?
Acute pericarditis is a condition referring to inflammation of the pericardial sac, lasting for less than 4-6 weeks.
What are 9 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
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
Describe 3 investigations for pericarditis
ECG changes
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
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
What is found if coronary / spinal arteries are involved in an aortic dissection? what if the distal aorta is involved?
coronary arteries → angina
spinal arteries → paraplegia
distal aorta → limb ischaemia
Can patients with pericarditis be managed as outpatients?
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
What is the treatment of pericarditis? 3
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
what is the chest pain type and findings in aortic dissection?
‘Tearing’ chest pain radiating through to the back
Unequal upper limb blood pressure
Shingles - does pain come first or rash?
Pain often precedes the rash
When does aortic dissection occur? where in the aorta is this found? who is this most common in?
This occurs when there is a flap or filling defect within the aortic intima. Blood tracks into the medial layer and splits the tissues with the subsequent creation of a false lumen. It most commonly occurs in the ascending aorta or just distal to the left subclavian artery (less common). The dissection may spread either proximally or distally with subsequent disruption to the arterial branches that are encountered. It is most common in Afro-carribean males aged 50-70 years.
What are 7 associations with 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 pulse found in aortic dissection
weak or absent carotid, brachial, or femoral pulse
variation (>20 mmHg) in systolic blood pressure between the arms
what is found when examining heart sounds of patients with aortic dissection? what happens to their blood pressure?
aortic regurgitation
hypertension
What is found on ECG of aortic dissection?
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
Describe the classification system for aortic dissection? how are they treated?
In the Stanford classification system the disease is classified into lesions with a proximal origin (Type A) and those that commence distal to the left subclavian (Type B).
Proximal (Type A) lesions are usually treated surgically, type B lesions are usually managed non operatively.
type A - ascending aorta, 2/3 of cases type B - descending aorta, distal to left subclavian origin, 1/3 of cases
What are the ECG findings of PE?
Diagnosis may be suggested by various ECG findings including S waves in lead I, Q waves in lead III and inverted T waves in lead III. Confirmation of the diagnosis is usually made through use of CT pulmonary angiography.
What is the typical history of a peptic ulcer?
Patients usually develop sudden onset of epigastric abdominal pain, it may be soon followed by generalised abdominal pain.
There may be features of antecendant abdominal discomfort, the pain of gastric ulcer is typically worse immediately after eating whereas eating may improve pain of duodenal ulcer
what is the diagnosis of peptic ulcer? how is this managed?
Diagnosis may be made by erect chest x-ray which may show a small amount of free intra-abdominal air (very large amounts of air are more typically associated with colonic perforation).
Treatment is usually with a laparotomy, small defects may be excised and overlaid with an omental patch, larger defects are best managed with a partial gastrectomy.
What is boerhaaves syndrome? where is this found? what is the history? what is a complication
Spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting.
The rupture is usually distally sited and on the left side.
Patients usually give a history of sudden onset of severe chest pain that may complicate severe vomiting.
Severe sepsis occurs secondary to mediastinitis.
What is the diagnosis of boerhaaves syndrome? how is this treated?
Diagnosis is CT contrast swallow.
Treatment is with thoracotomy and lavage, if less than 12 hours after onset then primary repair is usually feasible, surgery delayed beyond 12 hours is best managed by insertion of a T tube to create a controlled fistula between oesophagus and skin.
Delays beyond 24 hours are associated with a very high mortality rate.
When does chest pain warrant referral?
Referral
current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency admission chest pain 12-72 hours ago: refer to hospital the same-day for assessment chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action
What are the three features of anginal pain? what constitutes typical angina vs atypical angina vs non-anginal chest pain?
NICE define anginal pain as the following:
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
What are the investigations for angina?
For patients in whom stable angina cannot be excluded by clinical assessment alone NICE recommend the following (e.g. symptoms consistent with typical/atypical angina OR ECG changes):
1st line: CT coronary angiography 2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia) 3rd line: invasive coronary angiography
Give examples of non-invasive functional imaging?
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
What should all patients be offered who have angina?
all patients should receive aspirin and a statin in the absence of any contraindication
sublingual glyceryl trinitrate to abort angina attacks
What are 3 adverse effects of statins?
-myopathy: includes myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase. 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)
-liver impairment: the 2014 NICE guidelines recommend checking LFTs at baseline, 3 months and 12 months. Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range
-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
what are 2 contraindications to statins?
Contraindications
macrolides (e.g. erythromycin, clarithromycin) are an important interaction. Statins should be stopped until patients complete the course pregnancy
What 4 patient groups should be offered a statin?
Who should receive a statin?
all people with established cardiovascular disease (stroke, TIA, ischaemic heart disease, peripheral arterial disease) following the 2014 update, NICE recommend anyone with a 10-year cardiovascular risk >= 10% patients with type 2 diabetes mellitus should now be assessed using QRISK2 like other patients are, to determine whether they should be started on statins patients with type 1 diabetes mellitus who were diagnosed more than 10 years ago OR are aged over 40 OR have established nephropathy
What are the first line medications for angina?
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
What to do if there is a poor response to initial treatment of angina?
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
What calcium channel blockers should be used if in combination with a beta blockern to treat angina?
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)
What to do if a patient can’t tolerate the addition of a beta blocker/calcium channel blocker and they are on monotherapy for angina?
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
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.
What are 3 adverse effects of nicorandil? what is the contraindication to nicorandil;?
Adverse effects
headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration
Contraindications
left ventricular failure
When can a third drug be added in angina care?
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
What is the mechanism of action of nitrates?
Mechanism of action
nitrates cause the release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand
What are 4 side effects of nitrates?
ide-effects
hypotension tachycardia headaches flushing
what to do if patients get nitrate tolerance?
many patients who take nitrates develop tolerance and experience reduced efficacy
NICE advises that patients who take standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance
this effect is not seen in patients who take once-daily modified-release isosorbide mononitrate
Describe the use of adrenaline in ALS
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
Describe the use of amiodarone in ALS
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
What are th 4 ‘h’s reversible causes of cardiac arrest?
Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
What are th 4 ‘T’s reversible causes of cardiac arrest?
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade – cardiac
Toxins
What are the classical features of tamponade? what other features are seen? 6
Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure.
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
What is kussmauls sign?
Kussmaul’s sign describes a paradoxical rise in JVP during inspiration seen in constrictive pericarditis.
What is the difference between tamponade and constrictive pericarditis:
JVP
Pulsus paradoxus
Kussmaul’s sign
Characteristic features
JVP Absent Y descent /X + Y present
Pulsus paradoxus Present /Absent
Kussmaul’s sign Rare / Present
Characteristic features - /Pericardial calcification on CXR
How common is AF?
It is very common, being present in around 5% of patients over aged 70-75 years and 10% of patients aged 80-85 years
Describe the classification of AF
AF may by classified as either first detected episode, paroxysmal, persistent or permanent.
first detected episode (irrespective of whether it is symptomatic or self-terminating) recurrent episodes, when a patient has 2 or more episodes of AF. If episodes of AF terminate spontaneously then the term paroxysmal AF is used. Such episodes last less than 7 days (typically < 24 hours). If the arrhythmia is not self-terminating then the term persistent AF is used. Such episodes usually last greater than 7 days in permanent AF there is continuous atrial fibrillation which cannot be cardioverted or if attempts to do so are deemed inappropriate. Treatment goals are therefore rated control and anticoagulation if appropriate
What is used in rate controlling AF?
A beta-blocker or a rate-limiting calcium channel blocker (e.g. diltiazem) is used first-line to control the rate in AF.
If one drug does not control the rate adequately NICE recommend combination therapy with any 2 of the following:
a betablocker diltiazem (calcium channel blocker) digoxin
What is CHA2DS2-VASc score?
C Congestive heart failure 1
H Hypertension (or treated hypertension) 1
A2 Age >= 75 years 2
Age 65-74 years 1
D Diabetes 1
S2 Prior Stroke, TIA or thromboembolism 2
V Vascular disease (including ischaemic heart disease and peripheral arterial disease) 1
S Sex (female)
What CHA2DS2-VASc score suggests anticoagulation?
0 No treatment
1 Males: Consider anticoagulation
Females: No treatment (this is because their score of 1 is only reached due to their gender)
2 or more Offer anticoagulation
What is the orbit score?
Haemoglobin <130 g/L for males and < 120 g/L for females, or haemtocrit < 40% for males and < 36% for females 2
Age > 74 years 1
Bleeding history (GI bleeding, intracranial bleeding or haemorrhagic stroke) 2
Renal impairment (GFR < 60 mL/min/1.73m2) 1
Treatment with antiplatelet agents 1
What does the orbit score mean?
ORBIT score Risk group Bleeds per 100 patient-years
0-2 Low 2.4
3 Medium 4.7
4-7 High 8.1
How to cardiovert patients who’s AF has been less than 48hrs onset?
If the atrial fibrillation (AF) is definitely of less than 48 hours onset patients should be heparinised. Patients who have risk factors for ischaemic stroke should be put on lifelong oral anticoagulation. Otherwise, patients may be cardioverted using either:
electrical - 'DC cardioversion' pharmacology - amiodarone if structural heart disease, flecainide or amiodarone in those without structural heart disease
Following electrical cardioversion if AF is confirmed as being less than 48 hours duration then further anticoagulation is unnecessary
Describe the cardioversion process for patients with AF who have had this for longer than 48hrs
If the patient has been in AF for more than 48 hours then anticoagulation should be given for at least 3 weeks prior to cardioversion. An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded patients may be heparinised and cardioverted immediately.
NICE recommend electrical cardioversion in this scenario, rather than pharmacological.
If there is a high risk of cardioversion failure (e.g. Previous failure or AF recurrence) then it is recommend to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion
Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this time decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence
What is the management of AF following a stroke or TIA?
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 Clinical Knowledge Summaries 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
Who shouldn’t be offered rate control as a first line strategy in AF?
Rate control should be offered as the first‑line treatment strategy for atrial fibrillation except in people:
whose atrial fibrillation has a reversible cause who have heart failure thought to be primarily caused by atrial fibrillation with new‑onset atrial fibrillation (< 48 hours) with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm for whom a rhythm‑control strategy would be more suitable based on clinical judgement
What agents are used to maintain SR in patients with a history of AF?
Agents used to maintain sinus rhythm in patients with a history of atrial fibrillation
beta-blockers dronedarone: second-line in patients following cardioversion amiodarone: particularly if coexisting heart failure
Describe the anticoagulation in catheter ablation for AF
-prior to procedure
-post procedure
Anticoagulation
should be used 4 weeks before and during the procedure
it should be remember that catheter ablation controls the rhythm but does not reduce the stroke risk, even if patients remain in sinus rhythm. Therefore, patients still require anticoagulation as per their CHA2DS2-VASc score
if score = 0: 2 months anticoagulation recommended
if score > 1: longterm anticoagulation recommended
What are three complications of catheter ablation for AF?
cardiac tamponade
stroke
pulmonary vein stenosis
What is the success rate of catheter ablation for AF?
around 50% of patients experience an early recurrence (within 3 months) of AF that often resolves spontaneously
longer term, after 3 years, around 55% of patients who’ve had a single procedure remain in sinus rhythm. Of patients who’ve undergone multiple procedures around 80% are in sinus rhythm
Describe the ECG findings of atrial flutter
ECG findings
'sawtooth' appearance as the underlying atrial rate is often around 300/min the ventricular or heart rate is dependent on the degree of AV block. For example if there is 2:1 block the ventricular rate will be 150/min flutter waves may be visible following carotid sinus massage or adenosine
Describe the management of atrial flutter
Management
is similar to that of atrial fibrillation although medication may be less effective atrial flutter is more sensitive to cardioversion however so lower energy levels may be used radiofrequency ablation of the tricuspid valve isthmus is curative for most patients
What is the mechanism of action of amiodarone?
Amiodarone is a class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias. The main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)
What are 4 disadvantages of amiodarone?
The use of amiodarone is limited by a number of factors
very long half-life (20-100 days). For this reason, loading doses are frequently used should ideally be given into central veins (causes thrombophlebitis) has proarrhythmic effects due to lengthening of the QT interval interacts with drugs commonly used concurrently (p450 inhibitor) e.g. Decreases metabolism of warfarin numerous long-term adverse effects (see below)
Describe the monitoring of patients taking amiodarone
Monitoring of patients taking amiodarone
TFT, LFT, U&E, CXR prior to treatment TFT, LFT every 6 months
What are the adverse effects of amiodarone? 10
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
what is the acute management of SVT? what is used to prevent SVT?
Acute management
vagal manoeuvres:
Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe / carotid sinus massage
intravenous adenosine
rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
contraindicated in asthmatics - verapamil is a preferable option
electrical cardioversion
Prevention of episodes
beta-blockers radio-frequency ablation
What is the mechanism of action of warfarin?
Mechanism of action
inhibits epoxide reductase preventing the reduction of vitamin K to its active hydroquinone form this in turn acts as a cofactor in the carboxylation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.
What are the two indications for 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
what are 5 factors that can potentiate warfarin?
Factors that may potentiate warfarin
liver disease P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin cranberry juice drugs which displace warfarin from plasma albumin, e.g. NSAIDs inhibit platelet function: NSAIDs
How do you manage high INR with major bleeding
Stop warfarin
Give intravenous vitamin K 5mg
Prothrombin complex concentrate - if not available then FFP*
How do you manage INR >8 and mild bleeding?
Stop warfarin
Give intravenous vitamin K 1-3mg
Repeat dose of vitamin K if INR still too high after 24 hours
Restart warfarin when INR < 5.0
How do you managed INR >8 and no bleeding?
Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0
HOw do you manage INR 5-8 with mild bleeding?
Stop warfarin
Give intravenous vitamin K 1-3mg
Restart when INR < 5.0
How do you manage INR 5-8 with no bleeding?
Withhold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose
Name 7 inducers of P450 enzyme? what happens to INR?
INR decreases
antiepileptics: phenytoin, carbamazepine
barbiturates: phenobarbitone
rifampicin
St John’s Wort
chronic alcohol intake
griseofulvin
smoking (affects CYP1A2, reason why smokers require more aminophylline)
Name 11 P450 enxyme inhibitors |(INR increases)
antibiotics: ciprofloxacin, clarithromycine/erythromycin
isoniazid
cimetidine,omeprazole
amiodarone
allopurinol
imidazoles: ketoconazole, fluconazole
SSRIs: fluoxetine, sertraline
ritonavir
sodium valproate
acute alcohol intake
quinupristin
What are 4 side effects of warfarin?
haemorrhage
teratogenic, although can be used in breastfeeding mothers
skin necrosis
when warfarin is first started biosynthesis of protein C is reduced
this results in a temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration
thrombosis may occur in venules leading to skin necrosis
purple toes
What are 3 indications of DOAC?
prevention of stroke in non-valvular AF. NICE stipulate that certain other risk factors should be present. These are complicated and differ between the DOACs but generally require one of the following to be present:
prior stroke or transient ischaemic attack
age 75 years or older
hypertension
diabetes mellitus
heart failure
prevention of VTE following hip/knee surgery
treatment of DVT and PE
What is aortic regurgitation and what can cause this?
Aortic regurgitation (AR) is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole.
It can be caused either by disease of the aortic valve or by distortion or dilation of the aortic root and ascending aorta.
What are the 5 causes of aortic valve disease that present chronically as aortic regurgitation
rheumatic fever: the most common cause in the developing world
calcific valve disease
connective tissue diseases e.g. rheumatoid arthritis/SLE
bicuspid aortic valve (affects both the valves and the aortic root
What is the cause of aortic valve disease that presents acutely as aortic regurgitation?
infective endocarditis
What is the cause of aortic root disease that presents acutely as aortic regurgitation?
aortic dissection
What are the 5 causes of aortic root disease that present chronically as aortic regurgitation?
bicuspid aortic valve (affects both the valves and the aortic root)
spondylarthropathies (e.g. ankylosing spondylitis)
hypertension
syphilis
Marfan’s, Ehler-Danlos syndrome
What are 6 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
What is the investigation and management of aortic regurgitation?
Suspected AR should be investigated with echocardiography.
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
What are four features of symptomatic aortic stenosis?
chest pain
dyspnoea
syncope / presyncope (e.g. exertional dizziness)
murmur
an ejection systolic murmur (ESM) is classically seen in aortic stenosis
classically radiates to the carotids
this is decreased following the Valsalva manoeuvre
What are 8 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
What are 5 causes of aortic stenosis, which is most common?
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
Describe the management of aortic stenosis?
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
Describe the options for aortic valve replacement in aortic stenosis
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
Mitral regurgitation
-What is this?
-Is this common?
-What is the result of this if not treated?
Also known as mitral insufficiency, mitral regurgitation (MR) occurs when blood leaks back through the mitral valve on systole. It is the second most common valve disease after aortic stenosis. The mitral valve is located between the left atrium and ventricle, and regurgitation leads to a less efficient heart as less blood is pumped through the body with each contraction. This said, MR is common in otherwise healthy patients to a trivial degree and does not need treatment.
As the degree of regurgitation becomes more severe, the body’s oxygen demands may exceed what the heart can supply and as a result, the myocardium can thicken over time. While this may be benign initially, patients may find themselves increasingly fatigued as a thicker myocardium becomes less efficient, and eventually go into irreversible heart failure.
What are 7 risk factors of mitral regurgitation?
Risk factors
Female sex Lower body mass Age Renal dysfunction Prior myocardial infarction Prior mitral stenosis or valve prolapse Collagen disorders e.g. Marfan's Syndrome and Ehlers-Danlos syndrome
What are 5 causes of mitral regurgiation?
-Following coronary artery disease or post-MI: if the papillary muscles or chordae tendinae are affected by a cardiac insult, mitral valve disease may ensue as a result of damage to its supporting structures.
-Mitral valve prolapse: Occurs when the leaflets of the mitral valve is deformed so the valve does not close properly and allows for backflow. Most patients with this have a trivial degree of mitral regurgitation.
- Infective endocarditis: When vegetations from the organisms colonising the heart grow on the mitral valve, it is prevented from closing properly. Patients with abnormal valves are more likely to develop endocarditis as opposed to their peers.
-Rheumatic fever: While this is uncommon in developed countries, rheumatic fever can cause inflammation of the valves and therefore result in mitral regurgitation.
- Congenital
What are the signs and symptoms of MR?
Symptoms
Most patients with MR are asymptomatic, and patients suffering from mild to moderate MR may stay largely asymptomatic indefinitely. Symptoms tend to be due to failure of the left ventricle, arrhythmias or pulmonary hypertension. This may present as fatigue, shortness of breath and oedema.
Signs
The murmur heard on auscultation of the chest is typically a pansystolic murmur described as “blowing”. It is heard best at the apex and radiating into the axilla. S1 may be quiet as a result of incomplete closure of the valve. Severe MR may cause a widely split S2
What may be seen on CXR/ECG/Echo with MR?
Investigations
ECG may show a broad P wave, indicative of atrial enlargement Cardiomegaly may be seen on chest x-ray, with an enlarged left atrium and ventricle Echocardiography is crucial to diagnosis and to assess severity
What are the treatment options for MR?
Treatment options
Medical management in acute cases involves nitrates, diuretics, positive inotropes and an intra-aortic balloon pump to increase cardiac output If patients are in heart failure, ACE inhibitors may be considered along with beta-blockers and spironolactone In acute, severe regurgitation, surgery is indicated The evidence for repair over replacement is strong in degenerative regurgitation, and is demonstrated through lower mortality and higher survival rates When this is not possible, valve replacement with either an artificial valve or a pig valve is considered
What is mitral stenosis? what are the 4 causes?
Mitral stenosis describes the obstruction of blood flow across the mitral valve from the left atrium to the left ventricle. This leads to increases in pressure within the left atrium, pulmonary vasculature and right side of the heart.
It is said that the causes of mitral stenosis are rheumatic fever, rheumatic fever and rheumatic fever. Rarer causes that may be seen in the exam include mucopolysaccharidoses, carcinoid and endocardial fibroelastosis
What is rheumatic fever? what is the pathogenesis?
Rheumatic fever develops following an immunological reaction to a recent (2-4 weeks ago) Streptococcus pyogenes infection.
Pathogenesis
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
How is rheumatic fever diagnosed?
Diagnosis is based on evidence of recent streptococcal infection accompanied by:
2 major criteria 1 major with 2 minor criteria
What indicates recent strep. infection in the diagnosis of rheumatic fever?
Evidence of recent streptococcal infection
raised or rising streptococci antibodies, positive throat swab positive rapid group A streptococcal antigen test
What are 5 major criteria in the diagnosis of rheumatic fever?
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
What are 4 minor criteria in the diagnosis of rheumatic fever?
Minor criteria
raised ESR or CRP pyrexia arthralgia (not if arthritis a major criteria) prolonged PR interva
What is the management of rheumatic fever?
Outline of management
antibiotics: oral penicillin V anti-inflammatories: NSAIDs are first-line treatment of any complications that develop e.g. heart failure
what are 8 clinical features of MS?
dyspnoea
↑ left atrial pressure → pulmonary venous hypertension
haemoptysis
due to pulmonary pressures and vascular congestion
may range from pink frothy sputum to sudden haemorrhage secondary to rupture of thin-walled and dilated bronchial veins
mid-late diastolic murmur (best heard in expiration)
loud S1
opening snap
indicates mitral valve leaflets are still mobile
low volume pulse
malar flush
atrial fibrillation
secondary to ↑ left atrial pressure → left atrial enlargement
What features would indicate severe MS?
Features of severe MS
length of murmur increases opening snap becomes closer to S2
What is seen on CXR and echo in MS?
Chest x-ray
left atrial enlargement may be seen
Echocardiography
the normal cross-sectional area of the mitral valve is 4-6 sq cm. A 'tight' mitral stenosis implies a cross-sectional area of < 1 sq cm
What is the management of mitral stenosis in
-patients with AF
-Asymptomatic patients
-symptomatic patients
patients with associated atrial fibrillation require anticoagulation
currently warfarin is still recommended for patients with moderate/severe MS
there is an emerging consensus that direct-acting anticoagulants (DOACs) may be suitable for patients with mild MS who develop atrial fibrillation
asymptomatic patients
monitored with regular echocardiograms
percutaneous/surgical management is generally not recommended
symptomatic patients
percutaneous mitral balloon valvotomy
mitral valve surgery (commissurotomy, or valve replacement)
biological / bio-prosthetic valves
-What is the origin?
-What is a major disadvantage?
-is long term coag needed?
Usually bovine or porcine in origin
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
Mechanical heart valves
-What is the most common type?
-What is the advantage?
-What is the major disadvantage?
-Is anti-coag needed?
he most common type now implanted is the bileaflet valve. Ball-and-cage valves are rarely used nowadays
Mechanical valves have a low failure rate
Major disadvantage is the increased risk of thrombosis meaning long-term anticoagulation is needed.
What are the INR targets for mechanical heart valves?
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
What is balloon valvuloplasty?
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
What is the first line investigation for heart failure?
NICE issued updated guidelines on diagnosis and management in 2018. Previously the first-line investigation was determined by whether the patient has previously had a myocardial infarction or not this is no longer the case - all patients should have an N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test first-line.
Interpreting the test
if levels are 'high' arrange specialist assessment (including transthoracic echocardiography) within 2 weeks if levels are 'raised' arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks
What are normal/high/raised levels of BNP vs NTproBNP
BNP NTproBNP
High levels > 400 pg/ml (116 pmol/litre) > 2000 pg/ml (236 pmol/litre)
Raised levels 100-400 pg/ml (29-116 pmol/litre) 400-2000 pg/ml (47-236 pmol/litre)
Normal levels < 100 pg/ml (29 pmol/litre) < 400 pg/ml (47 pmol/litre)
What 11 things can increase BNP
Left ventricular hypertrophy
Ischaemia
Tachycardia
Right ventricular overload
Hypoxaemia (including pulmonary embolism)
GFR < 60 ml/min
Sepsis
COPD
Diabetes
Age > 70
Liver cirrhosis
What 6 things can decrease BNP
Obesity
Diuretics
ACE inhibitors
Beta-blockers
Angiotensin 2 receptor blockers
Aldosterone antagonists
What is the first line treatment for heart failure?
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
What is the second line treatment for heart failure?
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
What other drug can be used as an add on treatment for heart failure?
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
What are 5 third line therapies for heart failure?
Third-line treatment should be initiated by a specialist. Options include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy
What is ivabradine? what are 3 adverse effects?
Ivabradine is a class of anti-anginal drug which works by reducing the heart rate. It acts on the If (‘funny’) ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity.
Adverse effects
visual effects, particular luminous phenomena, are common headache bradycardia, heart block
when is ivabradine used for heart failure?
ivabradine
criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%
when is sacubitril-valsartan used for heart failure? (entresto)
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
When is digoxin used for heart failure?
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
when is hydralazine in combination with nitrate used for heart failure?
hydralazine in combination with nitrate
this may be particularly indicated in Afro-Caribbean patients or if unable to tolerate ACEI/ARB
When is cardiac resynchronisation therapy used for heart failure?
cardiac resynchronisation therapy
indications include a widened QRS (e.g. left bundle branch block) complex on ECG
What vaccines are used in heart failure?
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
What is used to classify severity of heart failure and describe the 4 classes?
The New York Heart Association (NYHA) classification is widely used to classify the severity of heart failure:
NYHA Class I
no symptoms
no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations
NYHA Class II
mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea
NYHA Class III
moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms
NYHA Class IV
severe symptoms
unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity
What is a loop diuretic?
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.
As loop diuretics work on the apical membrane they must first be filtered into the tubules by the glomerulus before they can have an effect. Therefore patients with poor renal function may require escalating doses to ensure a sufficient concentration is achieved within the tubules
What are two indications for loop diuretics?
Indications
heart failure: both acute (usually intravenously) and chronic (usually orally) resistant hypertension, particularly in patients with renal impairment
What are 9 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
How do thiazide diuretics work?
Thiazide diuretics work by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter. Potassium is lost as a result of more sodium reaching the collecting ducts. Thiazide diuretics have a role in the treatment of mild heart failure although loop diuretics are better for reducing overload. The main use of bendroflumethiazide was in the management of hypertension but recent NICE guidelines now recommend other thiazide-like diuretics such as indapamide and chlortalidone.
What are 8 common adverse effects of thiazide like diuretics?
Common adverse effects
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
What are 4 rare adverse effects of thiazide diuretics
thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis
What are 5 side effects of beta blockers?
bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction
What are 4 contraindications of beta blockers?
uncontrolled heart failure
asthma
sick sinus syndrome
concurrent verapamil use: may precipitate severe bradycardia
What is first-degree heart block?
First-degree heart block
PR interval > 0.2 seconds asymptomatic first-degree heart block is relatively common and does not need treatment
What is second-degree heart block?
Second-degree heart block
type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex
What is third-degree heart block?
Third-degree (complete) heart block
there is no association between the P waves and QRS complexes
What is brugada? how is it inherited? who is this more common in?
Brugada syndrome is a form of inherited cardiovascular disease with may present with sudden cardiac death. It is inherited in an autosomal dominant fashion and has an estimated prevalence of 1:5,000-10,000. Brugada syndrome is more common in Asians.
What is found on ECG with WPW? 4
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
How do you distinguish between type a and type b wpw?
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
What are 5 associations of WPW
Associations of WPW
HOCM mitral valve prolapse Ebstein's anomaly thyrotoxicosis secundum ASD
What is the treatment of WPW?
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
Describe the pathophysiology of brugada?
Pathophysiology
a large number of variants exist around 20-40% of cases are caused by a mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein
What is the most common form of cardiomyopathy?
Dilated cardiomyopathy
Describe the ECG changes found in brugada
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
What is the management of brugada?
Management
implantable cardioverter-defibrillator
What are primary cardiomyopathies?
Primary cardiomyopathies - predominately involving the heart
HOCM - Is this common? what causes this? what are the echo findings?
Leading cause of sudden cardiac death in young athletes
Usually due to a mutation in the gene encoding β-myosin heavy chain protein
Common cause of sudden death
Echo findings include MR, systolic anterior motion (SAM) of the anterior mitral valve and asymmetric septal hypertrophy
Autosomal dominant
Arrhythmogenic right ventricular dysplasia - What is this? what is the gene mutation? what is found on ECG? Is this autosomal dominant?
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
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
Autosomal dominant
HOCM and ARVD - what is the treatment?
ICD
What does mixed cardiomyopathy mean?
Mixed - rather confusingly most of the causes of dilated and restrictive cardiomyopathy are now listed separately in the ‘secondary’ causes. This category servers as a reminder that many patients will have a genetic predisposition to cardiomyopathy which is then triggered by the secondary process, hence the ‘mixed’ category
What are 4 classic causes of dilated cardiomyopathy?
Classic causes include
alcohol Coxsackie B virus wet beri beri doxorubicin
What is the pathophysiology of dilated cardiomyopathy?
dilated heart leading to predominately systolic dysfunction
all 4 chambers are dilated, but the left ventricle more so than right ventricle
eccentric hypertrophy (sarcomeres added in series) is seen
What are 4 features of dilated cardiomyopathy?
classic findings of heart failure
systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
S3
‘balloon’ appearance of the heart on the chest x-ra
What are classic causes of restrictive cardiomyopathy?
Classic causes include
amyloidosis post-radiotherapy Loeffler's endocarditis
What are two causes of acquired cardiomyopathy?
Peripartum cardiomyopathy and takutsubo
When does peripartum cardiomyopathy occur? who is this most common in?
Typical develops between last month of pregnancy and 5 months post-partum
More common in older women, greater parity and multiple gestations
What is takutsubo cardiomyopathy? what is seen on echo? what is treatment?
‘Stress’-induced cardiomyopathy e.g. patient just found out family member dies then develops chest pain and features of heart failure
Transient, apical ballooning of the myocardium
Treatment is supportive
What are infective causes of cardiomyopathy? 2
Coxsackie B virus
Chagas disease
What is an infiltrative cause of cardiomyopathy?
Amyloidosis
What is a cause of storage cardiomyopthy?
Haemochromatosis
What is a toxicity cause of cardiomyopathy? 2
Doxorubicin
Alcoholic cardiomyopathy
What is a granulomatous cause of cardiomyopathy?
Sarcoidosis
What are endocrine causes of cardiomyopathy? 3
Diabetes mellitus
Thyrotoxicosis
Acromegaly
what are neuromuscular causes of caridomyopthy? 3
Friedreich’s ataxia
Duchenne-Becker muscular dystrophy
Myotonic dystrophy
What nutritional deficiency can cause cardiomyopathy?
Beriberi (thiamine)
What is an autoimmune cause of cardiomyopathy?
Systemic lupus erythematosis
What is coarctation of 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.
What are four associations of co-arctation of aorta?
Associations
Turner's syndrome bicuspid aortic valve berry aneurysms neurofibromatosis
What are features of coarctation of aorta in infancy vs adults?
What is found on examination? 3
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
DVLA
-What are the rules for hypertension?
Specific rules
hypertension
can drive unless treatment causes unacceptable side effects, no need to notify DVLA
if Group 2 Entitlement the disqualifies from driving if resting BP consistently 180 mmHg systolic or more and/or 100 mm Hg diastolic or more
DVLA
-What are the rules for ACS / angina?
angioplasty (elective) - 1 week off driving
CABG - 4 weeks off driving
acute coronary syndrome- 4 weeks off driving
1 week if successfully treated by angioplasty
angina - driving must cease if symptoms occur at rest/at the wheel
DVLA
-What are the rules for pacemaker insertion?
pacemaker insertion - 1 week off driving
DVLA
-What are the rules for ICD?
mplantable cardioverter-defibrillator (ICD)
if implanted for sustained ventricular arrhythmia: cease driving for 6 months
if implanted prophylactically then cease driving for 1 month. Having an ICD results in a permanent bar for Group 2 drivers
DVLA
-What are the rules for successful catheter ablation for an arrythmia?
successful catheter ablation for an arrhythmia- 2 days off driving
DVLA
-What are the rules for aortic aneurysm?
aortic aneurysm of 6cm or more - notify DVLA. Licensing will be permitted subject to annual review.
an aortic diameter of 6.5 cm or more disqualifies patients from driving
DVLA
-What are the rules for heart transplant?
heart transplant: do not drive for 6 weeks, no need to notify DVLA
Endocarditis prophylaxis
-What should happen if patients at risk of endocarditis are undergoing gastro or GU investigations?
if a person at risk of infective endocarditis is receiving antimicrobial therapy because they are undergoing a gastrointestinal or genitourinary procedure at a site where there is a suspected infection they should be given an antibiotic that covers organisms that cause infective endocarditis
What is buergers disease?
What are the features 5
Buerger’s disease (also known as thromboangiitis obliterans) is a small and medium vessel vasculitis that is strongly associated with smoking.
Features
extremity ischaemia
intermittent claudication
ischaemic ulcers
superficial thrombophlebitis
Raynaud's phenomenon
what is takayasus arteritis?
Takayasu’s arteritis is a large vessel vasculitis. It typically causes occlusion of the aorta and questions commonly refer to an absent limb pulse. It is more common in younger females (e.g. 10-40 years) and Asian people.
what are 6 features of takayasus arteritis? what is an association?
Features
systemic features of a vasculitis e.g. malaise, headache unequal blood pressure in the upper limbs carotid bruit and tenderness absent or weak peripheral pulses upper and lower limb claudication on exertion aortic regurgitation (around 20%)
Associations
renal artery stenosis
What are the investigations and management for takayasu arteritis?
Investigations
vascular imaging of the arterial tree is required to make a diagnosis of Takayasu's arteritis
either magnetic resonance angiography (MRA) or CT angiography (CTA)
Management
steroids
Anticoagulation with antiplatelet meds
-What is done for patients who need Secondary prevention of stable cardiovascular disease with an indication for an anticoagulant
normally in this situation, all patients are recommended to be prescribed an antiplatelet
if an indication for anticoagulant exists (for example atrial fibrillation) it is indicated that anticoagulant monotherapy is given without the addition of antiplatelets
Anticoagulation with antiplatelet meds
-What is done for patients Post-acute coronary syndrome/percutaneous coronary intervention
in these patients, there is a much stronger indication for antiplatelet therapy
generally patients are given triple therapy (2 antiplatelets + 1 anticoagulant) for 4 weeks-6 months after the event and dual therapy (1 antiplatelet + 1 anticoagulant) to complete 12 months
there is variation from patient to patient however given that the stroke risk in atrial fibrillation varies according to risk factors.
Anticoagulation with antiplatelet meds
-What if a patient develops a PE on antiplatelets?
if a patient on antiplatelets develops a VTE they are likely to be prescribed anticoagulants for 3-6 months
an ORBIT score should be calculated. Those with a low risk of bleeding may continue antiplatelets. In patients with an intermediate or high risk of bleeding consideration should be given to stopping the antiplatelets
What are the 2 indications for dabigatran?
Firstly it is an option in the prophylaxis of venous thromboembolism following hip or knee replacement surgery.
Secondly, it is also licensed in the UK for prevention of stroke in patients with non-valvular atrial fibrillation who have one or more of the following risk factors present:
previous stroke, transient ischaemic attack or systemic embolism left ventricular ejection fraction below 40% symptomatic heart failure of New York Heart Association (NYHA) class 2 or above age 75 years or older age 65 years or older with one of the following: diabetes mellitus, coronary artery disease or hypertension
What is dabigatran?
Dabigatran is an oral anticoagulant that works by being a direct thrombin inhibitor. It is one of the drugs developed over the past 20 years as an alternative to warfarin, with the advantage that it does not require regular monitoring.
What are 2 side effects of dabigatran?
Unsurprisingly haemorrhage is the major adverse effect.
Doses should be reduced in chronic kidney disease and dabigatran should not be prescribed if the creatinine clearance is < 30 ml/min.
What can be used to reverse dabigatran
Idarucizumab cab be used for rapid reversal of the anticoagulant effects of dabigatran
What are 3 xanthomata types seen in hyperlipidaemia? what are these caused by?
Palmar xanthoma
remnant hyperlipidaemia
may less commonly be seen in familial hypercholesterolaemia
Eruptive xanthoma are due to high triglyceride levels and present as multiple red/yellow vesicles on the extensor surfaces (e.g. elbows, knees)
Causes of eruptive xanthoma
familial hypertriglyceridaemia
lipoprotein lipase deficiency
Tendon xanthoma, tuberous xanthoma, xanthelasma
familial hypercholesterolaemia
remnant hyperlipidaemia
What is xantholasma? how is this managed? 4
Xanthelasma are yellowish papules and plaques caused by localized accumulation of lipid deposits commonly seen on the eyelid. They are also seen in patients without lipid abnormalities.
Management of xanthelasma, options include:
surgical excision topical trichloroacetic acid laser therapy electrodesiccation
What is nictonic acid? what are the 3 adverse effects?
Nicotinic acid (niacin) is used in the treatment of patients with hyperlipidaemia, although its use is limited by side-effects. As well as lowering cholesterol and triglyceride concentrations it also raises HDL levels.
Adverse effects
flushing: mediated by prostaglandins impaired glucose tolerance myositis
What are 4 first line investigations of palpitations?
First-line investigations include:
-12-lead ECG: this will only capture the heart rhythm for a few seconds and hence is likely to miss episodic arrhythmias. However, other abnormalities linked to the underlying arrhythmia (for example a prolonged QT interval or PR interval, or changes suggesting recent myocardial ischaemia) may be seen.
-thyroid function tests: thyrotoxicosis may precipitate atrial fibrillation and other arrhythmias
-urea and electrolytes: looking for disturbances such as a low potassium
-full blood count
If the first line investigations are normal in patients c/o palpitations, what is the next step?
The most common investigation is Holter monitoring
portable battery operated device continuously records ECG from 2-3 leads usually done for 24 hours but may be used for longer if symptoms are less than daily patients are asked to keep a diary to record any symptomatic palpitations. This can later be compared to the rhythm strip at the time of the symptoms at the end of the monitoring a report is generated summarising a number of parameters including heart rate, arrhythmias and changes in ECG waveform
If no abnormality is found on holter monitor in patients c/o palpitations, what is the next step?
If no abnormality is found on the Holter monitor, and symptoms continue, other options include:
external loop recorder implantable loop recorder
How do thrombolytic drugs work? give three examples
Thrombolytic drugs activate plasminogen to form plasmin. This in turn degrades fibrin and help breaks up thrombi.
Examples
alteplase tenecteplase streptokinas
what are 8 contraindications to thrombolysis?
Contraindications to thrombolysis
active internal bleeding recent haemorrhage, trauma or surgery (including dental extraction) coagulation and bleeding disorders intracranial neoplasm stroke < 3 months aortic dissection recent head injury severe hypertension
What are three side effects of thrombolysis?
Side-effects
haemorrhage hypotension - more common with streptokinase allergic reactions may occur with streptokinase
ECG
-What is seen in ventricular and atrial hypertrophy?
Left ventricular hypertrophy
sum of S wave in V1 and R wave in V5 or V6 exceeds 40 mm
Right ventricular hypertrophy: the R:S. ratio in V1 greater than 1 is suggestive of right ventricular hypertrophy.
Left atrial enlargement
bifid P wave in lead II with a duration > 120 ms in V1 the P wave has a negative terminal portion
Right atrial enlargement
tall P waves in both II and V1 which exceed 0.25 mV
ECG changes with digoxin
down-sloping ST depression (‘reverse tick’, ‘scooped out’)
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia
What are the ECG changes with hypokalaemia?
ECG features of hypokalaemia
U waves small or absent T waves (occasionally inversion) prolong PR interval ST depression long QT
In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT
What are the ECG changes in LBBB and RBBB
One of the most common ways to remember the difference between LBBB and RBBB is WiLLiaM MaRRoW
in LBBB there is a 'W' in V1 and a 'M' in V6 in RBBB there is a 'M' in V1 and a 'W' in V6
What is long QT syndrome?
Long QT syndrome (LQTS) is an inherited condition associated with delayed repolarization of the ventricles. It is important to recognise as it may lead to ventricular tachycardia/torsade de pointes and can therefore cause collapse/sudden death. The most common variants of LQTS (LQT1 & LQT2) are caused by defects in the alpha subunit of the slow delayed rectifier potassium channel. A normal corrected QT interval is less than 430 ms in males and 450 ms in females.
What are two congenital causes of long QTS
Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
Romano-Ward syndrome (no deafness)
what are 7 drug causes of LQTS
-amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
-methadone
-chloroquine
-terfenadine**
-erythromycin
-haloperidol
-ondanestron
What are 6 non-drug and non-congenital causes of LQTS?
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
acute myocardial infarction
myocarditis
hypothermia
subarachnoid haemorrhage
What are 4 features of LQTS?
may be picked up on routine ECG or following family screening
Long QT1 - usually associated with exertional syncope, often swimming
Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli
Long QT3 - events often occur at night or at rest
sudden cardiac death
What is the management of LQTS? 3
Management
avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise) beta-blockers*** implantable cardioverter defibrillators in high risk cases
What causes the a wave in the JVP?
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
Describe the C / V / X descent / and Y descent of the JVP
‘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
What happens during S1 heart sound
S1
closure of mitral and tricuspid valves soft if long PR or mitral regurgitation loud in mitral stenosis
what happens during S2 heart sound?
S2
closure of aortic and pulmonary valves soft in aortic stenosis splitting during inspiration is normal
What happens in S3 heart sound?
S3 (third heart sound)
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
What happens in the S4 heart sounds
S4 (fourth heart sound)
may be heard in aortic stenosis, HOCM, hypertension
caused by atrial contraction against a stiff ventricle
therefore coincides with the P wave on ECG
in HOCM a double apical impulse may be felt as a result of a palpable S4
