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
