Cardiology Flashcards
What is the normal cardiac axis?
-30 degrees to +90 degrees
Between which angles is considered left axis deviation?
-30 to -90 degrees
Between which angles is considered right axis deviation?
+90 degrees to +180 degrees
Which leads are positive in the normal cardiac axis?
Lead I and II
What lead changes will be seen in left axis deviation?
I positive II negative
What lead changes are seen in right axis deviation?
I negative II positive
What ECG changes may be seen on a 15-lead ECG in a posterior STEMI?
ST elevation in V7-9
Reciprocal ST depression in V1-V3
What medications are used for secondary prevention post ACS?
ACEi/ARB (ramipril/candesartan) B-blocker (bisoprolol) Ticagrelor Aspirin Statin (atorvastatin)
What is the main cause of right axis deviation?
RVH
What can cause right ventricular hypertrophy?
Long standing hypoxia (COPD, pulmonary fibrosis) Structual defects in the heart Aortic stenosis Amyloidosis HTN Athletitism Hypertrophic cardiomyopathy
Why must significantly low magnesium be treated so agressively?
Severe hypomagnesaemia can cause ventricular arrhythmias
What causes left axis deviation?
left anterior fascicular block
left ventricular hypertrophy
What causes LVH most commonly?
HTN
What does right ventricular heave indicate?
RVH
What is the immediate management for a patient with Torsades de Pointes with no adverse features?
2g MgSO4 over 10 mins IV
What are roth spots?
Found in the eye
Caused by small retinal haemorrhages
Associated with multiple systemic conditions including endocarditis
How is WPW managed once treated acutely?
Catheter ablation of the accessory conduction pathway
What clinical features are characteristic of right sided heart failure?
Peripheral odema (pedal, scrotal, sacral)
Raised JVP
Hepatomegaly
Bloating
What clinical features are characteristic of left sided heart failure?
Cough
SOB
Paroxysmal nocturnal dyspnea
Orthopnea
Digoxin has a narrow therapeutic index. Acute digoxin toxicity maybe be potentiated by renal failure and hypokalaemia, for example following a recent gastroenteritis episode. What are the symptoms?
gastrointestinal disturbance (nausea, vomiting, abdominal pain), dizziness, confusion, blurry or yellow vision arrhythmias.
How might rhabdomyolysis cause an arrhythmia?
Myoglobin=nephrotoxic
Kidney insult
Hyperkalemia
What ECG changes may be present in hyperkalemia?
Tented T waves Prolonged QRS Slurring of ST segment Loss of p waves Asystole
How is the myocardium stabalised to prevent arrhythmias in hyperkalaemia?
10mls of 10% calcium gluconate over 5-10 mins
What is done to shift potassium back into the intracellular space in the treatment of hyperkaleamia?
IV fast acting insulin (actrapid)
10 units and IV glucose 50%
Sodium bicarbonate - 500mls 1/4% - only effective if patient is acidotic
5-10mg via nebulizer of salbutamol
How can potassium be eliminated from the body?
Calcium resonium - 15-45mg orally or rectally
Frusemide - 20-80mg depending on hydrations tatus
Dialysis
How is hypokalemia treated?
Replace magnesium
Oral K replacem% NaCl, dextrose induces further hypokalaemia)
What ECG changes may be seen in hypokalemia?
Small T waves U wave (after T) INcreased PR interval
First line treatment for hypercholestorleamia?
Atorvostatin
HMG-CoA reductase inhibitor
What is Beck’s triad?
Quiet heart sounds
HTN
Raised JVP
Seen in pericardial tamponade
Pharmacological management of HF with left ventricular systolic dysfunti?
ACE-i + B blocker
Second line is aldosterone antagonist e.g. sprinolactone
What signs may be seen on X-ray in a patient with heart failure?
ABCDE
Alevolar odema kerley B lines Cardiomegaly Dilated upper lobe vessels pleural Effusions
What murmurs may be heard on a patient with hypertrophic cardiomyopathy?
Ejection systolic murmur
loudest between lower sternal edge and apex, louder with exercise/standing/performing valsalva, quieter when sitting/squatting
Pansytolic murmur
loudest at the apex radiating to the axilla due to systolic anterior motion of the mitral valve
What does the murmur sound like in mitral regurgitation?
Holsystolic (pansystolic) / late systolic
Heard at the apex
with the diaphragm of the stethoscope when the patient is in the left lateral decubitus position
Radiates to the axilla
Louder on expiration
What does the murmur sound like in aortic stenosis?
Early diastolic murmur Heard loudest at the left sternal edge Radiates to carotid arteries crescendo-decrescendo Louder on expiration and leaning forward
First line management in stable angina?
beta blocker or rate limiting Calcium Chanel blocker
Short acting nitrate - GTN spray
What anti arrhythmatic drug commonly causes deranged TFTs?
Amiodarone
Examination findings suggestive of mitral valve prolapse?
Mid-systolic click
Systolic murmur suggestive of regurgitation
If symptomatic: dyspnoea, poor exercise tolerance, chest pain or palpitations secondary to AF
More common in patients with Marfan syndrome
What is the maximum safe rate of IV potassium replacement (to avoid an arrhythmia)?
10mmol/hour
Describe the murmur of mitral stenosis?
Mid-disastolic, loudest on expiration at the apex
Sometimes pliable valves have an audiable opening snap
How does a pericardial effusion appear on CXR?
Fluid may accumulate in the pericardial sac causing a globular appearance of the heart on a chest x-ray. This may occur following pericarditis or due to another cause such a malignancy.
What is a serious but rare complication of cardiac catheterisation?
Atheromatous debris can be scraped from the aortic wall causing cerebral, retinal, renal or GI emboli.
If a transthoracic echocardiograms cannot rule out a mass on a valve what should be done next?
A trans-oesophageal echocardiogram
What is the first line investigation for aortic stenosis?
Transthoracic echocardiogram
How does aortic stenosis cause syncope?
Calcification on the aortic leaflets
Cardiac output becomes fixed due to the obstruction and cannot meet with exertional demand leading to a fall in BP and therefore decreased brain perfusion
What is the most common isolated single valve lesion secondary to rheumatic heart disease?
Mitral stenosis
How does MS cause AF?
Stenosis lead to left atrial dilation which can lead to AF
What might cause exertional syncope?
Cardiac arrhythmia
What is a normal QT interval?
350-450ms
How should AF with adverse features such as HF and shock be treated?
Synchronised electrical cardioversion
In what condition does apical to radial pulse deficit occur and why?
Fast AF
Occurs as no all atrial impulses (palpable at apex) are mechanically conducted to the ventricles (palpable as peripheral pulse)
What does a cannon A wave on JVP waveform signafy?
Atrial contraction against a closed tricuspid valve during AV dissociation such as in this case of complete hear block
VT
Extrasytolese
What is an appropriate drug to control fast AF?
Bisoprolol (rate controling beta blocker)
Bisoprolol is a synthetic beta1-selective beta-adrenergic receptor blocker with a low affinity for beta2-receptors in bronchial smooth muscle, blood vessels, and fat cells and no intrinsic sympathomimetic activity.
Serious side effect of severe hypophosphataemia?
Arrythmias
Following a sucsessful angioplasty, for how long must a patient stop driving (EF>40 percent, no urgent interventions planned)
1 week
How is PCI performed?
Cardiac catheterisation via radial or femoral acsess
Over what time frame is PCI effective?
From 12h of onset of chest pain
When is PCI more effective than alteplase thrombolysis?
When it can be delivered within two hours of the time that the alteplase would be able to have been given
What length of time must a patient stop driving for after they have had an implantable cardiac defibrilator inserted for secondar prevention?
6 months
Defintive treatment of Brugada syndrome with ECG changes or symptoms?
Implantable cardiac defibrillator
What is Brugada sign?
Coved ST elevation >2mm with subsequent negative T waves
Management of asymptomatic mitral stenosis (MS) with no features of HF?
6 month monitoring (if stenosis progresses it can cause irreversable cardiac remodelling and must be treat promptly)
No medication
Management of an NSTEMI?
Dual antiplatelet therapy (aspirin 300mg, clopidogrel 300mg) GTN spray (Glyceryl Trinitrate spray)
When are fondaparinux (anticoagulant) or ticagrelor (antiplatelet) contraindicated?
Bleeding risks, use aspirin and clopidogerol instead
What does pleuretic chest pain and a mildly raised troponin which is not changing dynamically?
Pericarditis
What causes atrial flutter?
Regular and rapid contraction of the atria which are more frequent than the contractions of the ventricles, usually in a ratio of 2:1.
How does atrial flutter appear on ECG?
Sawtooth pattern
Acute myocraditis presentation?
Chest pain resembeling typical angina
Can present with ECG changes
Troponin release common
Patients may not fit the typical demorgraphics of patients with coronary artery disease (younger, female, minimal risk factors)
Patients sometimes have a history of precipitating viral illness
Where will ST elevation be seen in a STEMI involving the LAD?
V1-V4
Which vessels will be involved in a STEMI showing ST elevation in leads II, III, and aVF
RCA of LCx
Which leads may have ST elevation in a STEMI involving the LCx?
I
aVL
V5, V6
(II, III, avF)
Which ECG leads represent the lateral view?
I, aVL, V5, V6
Which ECG leads represent the inferior view?
II
III
aVF
Which ECG leads represent the anterior/septal view?
V1, V2, V3, V4
How should aortic stenosis causing symptoms OR with reduced ejection fraction be managed?
If able to tolerate open heart surgery: surgical aortic valve replacement
TAVR otherwise
For how long after an NSTEMI should a patient be anti-coagulated?
At least 48 hrs
LMWH such as enoxaparin 1mg/kg BD
What should metalic heart valves be anticoagulated with?
Warfarin
Cardiac complications of Marfan’s syndrome?
(aortic
dissection and regurgitation)
What management to patients at risk of or with complere heart block require?
Permanent pacing
How should Mobitz type II be managed?
Permanent pacing due to risk of complete heart block and becoming haemodynamically unstable
Initial management of acute bradycardia?
ADBCDE, ECG monitoring, reverse any obvious cause
If adverse features (shock, syncope, myocardial ischemia, HF) then atroping 500mcg IV is given (repeat boluses up to 3mg)
How does atropine IV 500mcg (up to 3mg in total boluses) treat acute bradycardia?
Atropine blocks the vagus nerve activity on the heart, which increases the firing rate at the SA node
Factors which might increase the risk of asystole in bradycardia?
Mobitz Type II block
Complete heart block + broad QRS
Recent asystole
Ventricular phase > 3 seconds
What is the best diagnostic test for HF?
Congestive cardiac funny
How can anaemia cause high output cardiac failure?
Decreased oxygen carrying capacitym heart compensates by increasing CO initially. The heart eventually undergoes remodelling and subsequent decompensation such that CO is decreased to below the normal level
Causes of high output heart failure?
(Increases metabolic demands)
Pregnancy
Thyrotoxicosis
Anaemia
Initial treatment for hyperkalemia with ECG changes?
10ml 10% calcium gluconate IV
What ECG changes - that are not associated with toxicity - may occur in patients with digoxin?
widespread downsloping ST segments
What are the indications for DC cardioversion in a patient with tachycardia?
Shock
Myocardial ischemia
Syncope
Heart failure
What is IV adenosine used for?
Tachycardia
Which region of the heart does the RCA supply?
Posterior aspects of the left ventricle (correlates to II, III and avF)
What medication can be used to manage HTN crisis?
- Short acting ACEi
e.g. captopril
Followed by conversion to long acting ACEi
2nd line: Calcium channel blockers
Dialysis can be used for patients who are failing to respond
For a patient with heart failure secondary to symptomatic mitral regurgitation?
Mitral valve repair
Describe the murmur heard in mitral regurg?
Pan-systolic murmur
Radiates to axilla
Louder on expiration
What ECG changes are seen in hypokalemia?
U waves - humps following inverted waves
Seen in multiple leads
What is Dressler’s syndrome?
Acute pericarditis occuring weeks following MI (or any damage to heart tissue/pericardium)
Widespread upward sloping ‘‘saddle shaped’’ ST elevation
PR depression
Spodick’s sign - downward sloping T-P line
Most appropriate management of a stable patient with VT?
Amiodarone, 300mg IV loading dose over 20-60 mins
900mg of amiodarone over 24 hours
How does amiodarone terminate ventricular rhythm?
It is a anti-dysrhythmic drug as well as a rate-limiting drug
In the diagnosis of infective endocarditis, what the major Dukes criteria?
Positive blood culture results for IE
Evidence of endocardial involvement from echocardiography
New valvular regurgitation
In the diagnosis of infective endocarditis, what are the minor Duke’s criteria?
Vascular phenomena (Janeway’s lesions)
Immunological phenomena (Osler’s nodes, Roth spots, Ostlers nodes, +RF)
One positive blood culture (for organisms not meeting major criteria)
Fever
Criteria to fufil to diagnose endocarditis?
2x Dukes major OR
5x Dukes minor OR
1x major x3 minor
What is normal R wave progression?
The R wave should be small in lead V1. Throughout the precordial leads (V1-V6), the R wave becomes larger — to the point that the R wave is larger than the S wave in lead V4. The S wave then becomes quite small in lead V6; this is called “normal R wave progression.”
What is poor R wave progression?
When the R wave remains small in leads V3 to V4 — that is, smaller than the S wave — the term “poor R wave progression” is used.
What is atheroclerosis?
Combination of atheromas - fatty depositis in the artery walls and sclerosis (the process of hardening or stiffening of the blood vessel walls)
Which arteries are affected by atherosclerosis?
Medium and large
Pathophysiology of atherosclerosis?
Chronic inflammation + activation of the immune system in the artery wall
Deposition of lipids in the artery wall
Development of fibrous atheramatous plaques, causing
1.Stiffening of the artery walls leading to hypertension and strain on the heart as it pumps against the resistance
2. Stenosis leading to reduced blood flow (angia)
3. Plaque rupture giving off a thrombus that blocks a distal vessel leading to ischemia, for example ACS
Modifiable risk factors for atherosclerosis?
Smoking Alcohol consumption Poor diet (high sugar and transfat, low fruit veg and omega 3 consumption) Low exercise Obestity Poor sleep Stress
Non-modifiable risk factors?
Older age
Family history
Male
Medical co-morbidities that increase risk of atheroslerosis (and therefore should be carefully managed)
Diabetes Hypertension Chronic kidney disease Inflammatory conditions, such as rheumatoid arthritis Atypical antipsychotic medications
Complications secondary to atheroslerosis?
Angina Myocardial Infarction Transient Ischaemic Attacks Stroke Peripheral Vascular Disease Mesenteric Ischaemia
Types of CVD prevention?
Primary - for patients who have never had CVD in the past
Secondary - pts who have had angina, MI, TIA, stroke, peripheral vascular
What can be done to optomise modifiable risk factors in patients with CVD?
Advice on diet, exercise and weight loss
Stop smoking
Stop drinking alcohol
Tightly treat co-morbidities (such as diabetes)
What is Q risk 3?
Perform a QRISK 3 score. This will calculate the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years. If they have more than a 10% risk of having a stroke or heart attack over the next 10 years (i.e. their QRISK 3 score is above 10%) then you should offer a statin (current NICE guidelines are for atorvastatin 20mg at night).
Which patients should be offered atorvastatin 20mg?
QRISK score 3 + (after 6 months lifestyle changes attempted)
CKD for more than 10 years
Type 1 diabetics for more than 10 years
How should statins, when started, be monitored?
NICE recommend checking lipids at 3 months and increasing the dose to aim for a greater than 40% reduction in non-HDL cholesterol. Always check adherence before increasing the dose.
NICE also recommend checking LFTs within 3 months of starting a statin and again at 12 months. They don’t need to be checked after that if they are normal. Statins can cause a transient and mild rise in ALT and AST in the first few weeks of use and they often don’t need stopping if the rise is less than 3 times the upper limit of normal.
What change in cholesterol does a statin aim for?
greater than 40% reduction in non-HDL cholesterol
What is the AAAA secondary prevention of CVD?
Aspirin (+ second antiplatelet such as clopidogrel for 12 months) Atorvastatin 80mg Atenolol (or another beta blocker - bisoprolol, titrated to maximum tolerated dose) ACE inhibitor (commonly ramipril) titrated
Notable side effects of statins?
Myopathy (check creatine kinase in patients with muscle pain or weakness)
Type 2 diabetes
Haemorrhagic strokes (very rarely)
Pathophysiology of angina?
A narrowing of the coronary arteries reduces blood flow to the myocardium (heart muscle). During times of high demand such as exercise there is insufficient supply of blood to meet demand. This causes symptoms the symptoms of angina, typically constricting chest pain with or without radiation to jaw or arms.
Stable angina vs unstable angina?
Angina is “stable” when symptoms are always relieved by rest or glyceryl trinitrate (GTN). It is “unstable” when the symptoms come on randomly whilst at rest, and this is considered as an Acute Coronary Syndrome.
Gold standard investigation for angina?
CT coronary angiogram
Contrast injected, CT images taken when heart beats to give a detailed view of the coronary arteries, highlighting any narrowin
What baseline investigations should be?
Physical Examination (heart sounds, signs of heart failure, BMI) ECG FBC (check for anaemia) U&Es (prior to ACEi and other meds) LFTs (prior to statins) Lipid profile Thyroid function tests (check for hypo / hyper thyroid) HbA1C and fasting glucose (for diabetes)
Management of angina?
R – Refer to cardiology (urgently if unstable, if not just refer to rapid asses chest pain clinic)
A – Advise them about the diagnosis, management and when to call an ambulance
M – Medical treatment - immediate symptomatic, long term symptomatic, secondary prevention of CVD
P – Procedural or surgical interventions
Immediate symptomatic relief of angina (medical angina)
Their GTN spray is used required. It causes vasodilation and helps relieves the symptoms.
Take GTN, then repeat after 5 minutes. If there is still pain 5 minutes after the repeat dose – call an ambulance.
First line pharmacutical management of angina?
Beta blocker (e.g. bisoprolol 5mg once daily) or;
Calcium channel blocker (e.g. amlodipine 5mg once daily)
Or both if symptoms not controlled on one
Or second line
Second line medications for long term symptomatic relief of angina?
Long acting nitrates (e.g. isosorbide mononitrate)
Ivabradine
Nicorandil
Ranolazine
Secondary prevention of CVD in patients with angina (medications)
Aspirin (i.e. 75mg once daily)
Atorvastatin 80mg once daily
ACE inhibitor
Should already be on a beta-blocker for symptomatic relief.
What procedual interventions could a patient with angina potentially undergo?
Percutaneous Coronary Intervention PCI with coronary angioplasty - proximal or extensive disease
Coronary artery bypass graft (CABG) -severe stenosis
What does PCI with coronary angioplasty involve?
This involves putting a catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance and injecting contrast so that the coronary arteries and any areas of stenosis are highlighted on the xray images. This can then be treated with balloon dilatation followed by insertion of a stent.
What arteries might be used in PCI?
Femoral
Brachial
What does a conronary artery bypass graft involve (CABG)?
This involves opening the chest along the sternum (causing a midline sternotomy scar), taking a graft vein from the patient’s leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis. The recovery is slower and the complication rate is higher than PCI.
What vein is usually used to make a graft during a CABG?
Great saphenous vein
Where will a patient undergoing PCI end up with scaring?
Brachial artery access
Femoral artery access
Where will a patient CABG have a scar?
Midline sternotomy
Great saphenous vein harvesting
What causes ACS?
Acute Coronary Syndrome is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery. When a thrombus forms in a fast flowing artery it is made up mostly of platelets. This is why anti-platelet medications such as aspirin, clopidogrel and ticagrelor are the mainstay of treatment.
What anti-platelet medications are used to treat ACS?
Aspirin
Clopidogrel
Ticagrelor
What does the right coronary artery supply?
Curves around the right side under the heart and supplies: Right atrium Right ventricle Inferior aspect of left ventricle Posterior septal area
What does the cirumflex artery supply?
Curves around the top, left and back of the heart to supply:
Left atrium
Posterior apsect of left ventricle
What does the LAD supply?
Travels down the middle of the heart and supplies:
Anterior aspect of left ventricle
Anterior aspect of septum
Three types of ACS
Unstable Angina
ST Elevation Myocardial Infarction (STEMI)
Non-ST Elevation Myocardial Infarction (NSTEMI)
Which coronary arteries are branches of the left coronary artery?
Circumflex artery
Left anterior descending artery
What is the left coronary artery responsible for supplying?
Left atrium
Posterior and anterior aspects of the left ventricle
Anterior aspect of the septum
What ECG changes are diagnostic of STEMI?
ST elevation OR
New left bundle branch block
What should be done when suspecting ACS when an ECG has no ST elevation or new bundle branch block?
If there are raised troponin levels and/or other ECG changes (ST depression or T wave inversion or pathological Q waves) the diagnosis is NSTEMI
If troponin levels are normal and the ECG does not show pathological changes the diagnosis is either unstable angina or another cause such as musculoskeletal chest pain
What additional leads are required if an ECG shows ST depression in the anterior leads (V3, V4)?
V7, V8, V9
ACS symptoms?
Symptoms occur at rest and last over 20 mins: Nausea and vomiting Sweating and clamminess Feeling of impending doom Shortness of breath Palpitations Pain radiating to jaw or arms
Which patients typically suffer silent MIs?
Diabetic patients
ECG changes in an NSTEMI?
ST segment depression in a region
Deep T Wave Inversion
Pathological Q Waves (suggesting a deep infarct – a late sign)
ECG lead I, aVL and V3-V6 represent which coronary artery and which area of the heart?
Left coronary artery
Anterolateral
Blood supply to anterolateral heart?
LCA
Leads V1-V4 represent which coronary artery and which area of the heart?
LAD
Anterior
What coronary artery supplies the anterior heart?
LAD
ECG leads I, aVL and V5-V6 represent which coronary artery and which area of the heart??
Circumflex artery
Lateral
Which artery supplies blood to the lateral side of the heart?
Circumflex
ECG leads II, III and aVF represent which coronary artery and which area of the heart?
Right coronary artery
Inferior
Which coronary artery supplies the inferior heart?
Right coronary artery
Troponins are proteins found in cardiac muscle, which can rise in myocardial ischemia as the proteins are released from the ischemic muscle. What can cause them other than ACS?
Chronic renal failure Sepsis Myocarditis Aortic dissection Pulmonary embolism
What pattern of troponin is consistent with MI?
Serial troponins measured: baseline, 6 or 12 hours after onset of symptoms)
Continue to rise
Investigations, other than ECG and troponins, for suspected ACS?
Physical Examination (heart sounds, signs of heart failure, BMI) ECG FBC (check for anaemia) U&Es (prior to ACEi and other meds) LFTs (prior to statins) Lipid profile Thyroid function tests (check for hypo / hyper thyroid) HbA1C and fasting glucose (for diabetes) Plus:
Chest xray to investigate for other causes of chest pain and pulmonary oedema
Echocardiogram after the event to assess the functional damage
CT coronary angiogram to assess for coronary artery disease
When should primary PCI be used in a STEMI?
If it is available within 2 hours of presentation
When should thrombolysis be used in a STEMI?
If PCI is not available within two hours of presentation
Examples of thrombolytic agents?
Streptokinase
Alteplase
Tenecteplase
How is an NSTEMI treated acutely?
BATMAN
Beta blockers (unless contraindicated)
Aspirin - 300mg stat dose
Ticaglrelor 180mg stat dose/clopidogrel 300mg if high bleeding risk
Morphine - titrated to control pain
Anticoagulant - fondaparinux (unless high bleeding risk)
Nitrates (e.g.) GTN to relieve coronary artery spasam
What anticoagulant is used to acutely manage NSTEMI?
Fondaparinux, unless high bleeding risk
What is the GRACE score used to asses?
Indication for PCI following an MI
<5% Low Risk
5-10% Medium Risk - consider early PCI (within 4 days of admission) to treat underlying coronary artery disease)
>10% High Risk - consider early PCI (within 4 days of admission) to treat underlying coronary artery disease)
Complications of MI?
DREAD Death Rupture of heart septum or papillary muscles Edema (HF) Arrhythmia and Aneurysm Dressler's syndrome
What is Dressler’s syndrome?
This is also called post-myocardial infarction syndrome. It usually occurs around 2-3 weeks after an MI. It is caused by a localised immune response and causes pericarditis (inflammation of the pericardium around the heart).
How does Dressler’s syndrome present?
2-3 weeks after MI
Pleuretic chest pain
Low grade fever
Pericardial rub Pericardial effusion/(tamponade)
How is Dressler’s syndrome diagnosed?
A diagnosis can be made with an ECG (global ST elevation and T wave inversion),
Echocardiogram (pericardial effusion) and
Raised inflammatory markers (CRP and ESR).
How is Dressler’s syndrome managed?
NSAIDs (aspirin/ibuprofen)
Steroids if more severe (prednisolone)
May need pericardiocentesis
Secondary Prevention Medical Management (6 As) of ACS?
Aspirin 75mg once daily
Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)
Atenolol (or other beta blocker titrated as high as tolerated)
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
Dual antiplatelet duration will vary following PCI procedures depending on the type of stent that was inserted. This is due to a higher risk of thrombus formation in different stents.
Lifetsyle interventions to prevent ACS?
Stop smoking
Reduce alcohol consumption
Mediterranean diet
Cardiac rehabilitation (a specific exercise regime for patients post MI)
Optimise treatment of other medical conditions (e.g. diabetes and hypertension)
What is a type 1 MI?
MI due to an acute coronary event
What is a type 2 MI?
Ischemia secondary to increased demand or reduced supply of oxygen (e.g. severe anaemia, tachycardia, hypotension)
What is a type 3 MI?
Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
What is a type 4 MI?
MI associated with PCI / coronary stunting / CABG
How does acute left ventricular failure cause pulmonary odema?
Left ventricle is unable to adequately move blood through the left side of the heart and out into the body.
This causes a backlog of blood that increases the amount of blood stuck in the left atrium, pulmonary veins and lungs.
As the vessels in these areas are engorged with blood due to the increased volume and pressure they leak fluid and are unable to reabsorb fluid from the surrounding tissues.
This causes pulmonary oedema, which is where the lung tissues and alveoli become full of interstitial fluid.
This interferes with the normal gas exchange in the lungs, causing shortness of breath, oxygen desaturation and the other signs and symptoms.
What is pulmonary odema?
lung tissues and alveoli become full of interstitial fluid as the pulmonary vessels become engorged with blood so leak fluid and are unable to reabsorb fluid
What might trigger acute left ventricular failure?
Iatrogenic (e.g. aggressive IV fluids in frail elderly patient with impaired left ventricular function)
Sepsis
Myocardial Infarction
Arrhythmias
How might acute left ventricular failure present?
Acute LVF typical presents as a rapid onset breathlessness. This is exacerbated by lying flat and improves on sitting up.
- SOB + increased RR
- Looking and feeling unwell
- Productive cough with white/pink sputum
What might be found on examination of a patient with left sided heart failure?
Increased RR
Reduced O2 sats
Tachycardia
3rd Heart sound
Bilateral basal crackles (sounding wet) on ascultation
Hypotension in severe cases (cardiogenic shock)
What signs and symptoms may be associated in patients with acute LVF that are associated with the underlying cause?
Chest pain in ACS
Fever in sepsis
Palpitations in arrhythmias
Findings on examination of a patient with right sided heart failure?
Raised Jugular Venous Pressure (JVP) (a backlog on the right side of the heart leading to an engorged jugular vein in the neck) Peripheral oedema (ankles, legs, sacrum)
Work up in suspected HF?
History
Clinical Examination
ECG (to look for ischaemia and arrhythmias)
Arterial Blood Gas (ABG)
Chest Xray
Bloods (routine bloods for infection, kidney function, BNP and consider troponin if suspecting MI)
What is B-type Natriuretic Peptide?
Hormone released from heart ventricles when the myocardium is stretched beyond the normal range.
High BNP indicated the heart if overloaded with blood beyond its normal capacity to pump effectively
What is the action of BNP?
Relax the smooth muscle in the blood vessels, reducing systemic vascular resitance making it easier for the heart to pump blood through the ystem.
Acts on kidneys as a diuretic to promote the excretion of more water in the urine.
This reduced the circulation volume helping to improve the function of the heart.
Sensitivity of BNP in diagnosis of HF?
High
Negative is useful in ruling out heart failure
Specificity of BNP in diagnosing HF?
Low
A positive result can have other causes
Causes of raised B-type Natriuretic Peptide (BNP)
HF Tachycardia Sepsis PE Renal impairment COPD
What is the main measure of left ventricular function?
Ejection fraction
How can ejection fraction be assesed?
Echocardiogram
What is meant by ejection fraction?
Percentage of blood in the left ventricle that is squeezed out with each ventricular contraction
What is considered a normal ejection fraction?
50% of higher
Chest X ray findings in LVF?
Cardiomegaly (cardiace silhouette is more than half the diameter of the widest part of the lung fields - cardiac thoracic ratio of over 0.5)
Upper lobe venousdiversion
Bilateral pleural effusions (fluid leaking from odematous lung tissue)
Fluid in the interlobular fissures (Fluid leaking from oedematous lung tissue)
Fluid in the septal lines (kerley lines)
How is acute LVF managed?
Pour SOD
Pour away (stop) their IV fluids
Sit up (when lying flat fluid in the lungs spreads to a larger area, sitting up takes fluid to bases leaving upper lungs clear for gas exchange)
Oxygen (if sats<95%)
Diuretics (IV furosemide 40mg stat, reducing circulation volume and means the heart is less overloaded allowing it to pump more effectively)
What MUST be monitored in a patient with acute lVF?
Monitor fluid balance. Measuring fluid intake, urine output, U&E bloods and daily body weight is essential to balance their fluid input and output.
Other options in LVF to consider in severe acute pulmonary oedema or cardiogenic shock (not routinely used) include:
Intravenous opiates (opiates such as morphine act as vasodilators but are not routinely recommended).
Non-Invasive Ventilation (NIV). Continuous Positive Airway Pressure (CPAP) involves using a tight fitting mask to forcefully blow air into their lungs. This helps to open the airways and alveoli to improve gas exchange. If NIV does not work they may need full intubation and ventilation.
“Inotropes”, for example an infusion of noradrenalin. Inotropes strengthen the force of heart contractions and improve heart failure, however they need close titration and monitoring, so by this point you would need to send the patient to the local coronary care unit / high dependency unit / intensive care unit.
What type of respiratory failure does acute LVF cause?
Type 1 respiratory failure
low O2 without increase in blood CO2
How might chronic HF present?
Breathlessness worsened by exertion
Cough. They may produce frothy white/pink sputum.
Orthopnoea (the sensation of shortness of breathing when lying flat, relieves by sitting or standing). Ask them how many pillows they use at night.
Paroxysmal Nocturnal Dyspnoea
Peripheral oedema (swollen ankles)
What is paroxysmal nocturnal dyspnoea (PND)?
Paroxysmal nocturnal dyspnoea is a term used to describe the experience that patients have of suddenly waking at night with a severe attack of shortness of breath and cough.
Sitting up or walking will help patient to get their breath back
Symptoms improve over several mins
What causes PND?
- Fluid settling across a large SA of their lungs as they lie flat so gas exhange in lungs is inefficient
- During sleep the respiratory centre in the brain becomes less responsive so their RR and effort doesn’t increase in response to reduce O2 sat as it would when awake. This causes more significant pulmonary congestion and hypoxia to develop.
- Less adrenalin circulates during sleep, so myocardium is more relaxed and CO is reduced
How is chronic heart failure diagnosed?
Clinical presentation
BNP blood test (specifically “N-terminal pro-B-type natriuretic peptide” – NT‑proBNP)
Echocardiogram
ECG
Causes of HF?
Ischaemic Heart Disease
Valvular Heart Disease (commonly aortic stenosis)
Hypertension
Arrhythmias (commonly atrial fibrillation)
What NT-proBNP warrents urgent referal?
NT-proBNP > 2,000 ng/litre warrants urgent referral
Management of acute HF?
Refer to specialist (NT-proBNP > 2,000 ng/litre warrants urgent referral)
Careful discussion and explanation of the condition
Medical management (see below)
Surgical treatment in severe aortic stenosis or mitral regurgitation
Heart failure specialist nurse input for advice and support
Additional management:
Yearly flu and pneumococcal vaccine
Stop smoking
Optimise treatment of co-morbidities
Exercise at tolerated
Medical treatmeant for chronic HF?
ABAL
ACE inhibitor (e.g. ramipril titrated as tolerated up to 10mg once daily)/ARB (e.g. candesartan up to 32mg OD)
Beta Blocker (e.g. bisoprolol titrated as tolerated up to 10mg once daily)
Aldosterone antagonist when symptoms not controlled with A and B and rEF (spironolactone or eplerenone)
Loop diuretics improves symptoms (e.g. furosemide 40mg once daily)
N.B. Patients should have their U&Es monitored closely whilst on diuretics, ACE inhibitors and aldosterone antagonists as all three medications can cause electrolyte disturbances.
What is Cor Pulmonale?
Cor pulmonale is right sided heart failure caused by respiratory disease.
Pathophysiology of Cor pulmonalae?
The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) results in the right ventricle being unable to effectively pump blood out of the ventricle and into the pulmonary arteries.
This leads to back pressure of blood in the right atrium, the vena cava and the systemic venous system.
Causes of Cor Pulmonale?
COPD is the most common cause Pulmonary Embolism Interstitial Lung Disease Cystic Fibrosis Primary Pulmonary Hypertension
How might patients present with Cor Pulmonale?
SOB - patients may attribute this to underlying lung pathology Peripheral odema Increase SOBOE Syncope (diziness or fainting) Chest pain
What might be remarkable when examining a patient with Cor Pulmonale?
Hypoxia
Cyanosis
Raised JVP (due to a back-log of blood in the jugular veins)
Peripheral oedema
Third heart sound
Murmurs (e.g. pan-systolic in tricuspid regurgitation)
Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)
What type of HF may warrent LTOT?
Cor Pulmonale
What is essential HTN?
Primary HTN
HTN has developed on its own without secondary cause
Secondary causes of HTN?
ROPE
R – Renal disease. This is the most common cause of secondary hypertension. If the blood pressure is very high or does not respond to treatment consider renal artery stenosis.
O – Obesity
P – Pregnancy induced hypertension / pre-eclampsia
E – Endocrine. Most endocrine conditions can cause hypertension but primarily consider hyperaldosteronism (“Conns syndrome”) as this may represent 2.5% of new hypertension. A simple test for this is a renin:aldosterone ratio blood test.
When a patient is newly diagnosed with HTN, when should specialist investigations be considered?
Specialist investigations should be considered in patients with a potential secondary cause for their hypertension or aged under 40 years.
Key complications of HTN?
Ischaemic heart disease Cerebrovascular accident (i.e. stroke or haemorrhage) Hypertensive retinopathy Hypertensive nephropathy Heart failure
How often should blood pressure be measured to screen for HTN?
Every 5 years
OR more often in patients that are on borderline for diagnosis
Annually in patients with T2DM
Which patients should have 24 hour ambulatory blood pressure or home readings to confirm HTN and exclude white coat syndrome?
Patients with a clinic blood pressure between 140/90 mmHg and 180/120 mmHg
What is the white coat effect?
The white coat effect is defined as more than a 20/10 mmHg difference in blood pressure between clinic and ambulatory or home readings.
Which reading should be used when BP is measured in both arms?
if the difference is more than 15 mmHg using the reading from the arm with the higher pressure
Stage 1 HTN is defined as what?
Clinic reading >140/90
Ambulatory/Home readings >135/85
Stage 2 HTN is defined as what?
Clinic reading >160/100
Ambulatory/home readings >150/95
Stage 3 HTN is defined as what?
BP >180/120
Patients with a new diagnosis of HTN should be screened for end organ damage - how?
Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage
Bloods for HbA1c, renal function and lipids
Fundus examination for hypertensive retinopathy
ECG for cardiac abnormalities
Which medications can be used to treat HTN?
A – ACE inhibitor (e.g. ramipril 1.25mg up to 10mg once daily)
B – Beta blocker (e.g. bisoprolol 5mg up to 20mg once daily)
C – Calcium channel blocker (e.g. amlodipine 5mg up to 10mg once daily)
D – Thiazide-like diuretic (e.g. indapamide 2.5mg once daily)
ARB – Angiotensin II receptor blocker (e.g. candesartan 8mg to up 32mg once daily)
To which patients with HTN is medical management offered to?
All patients with stage 2 hypertension
All patients under 80 years old with stage 1 hypertension that also have a Q-risk score of 10% or more, diabetes, renal disease, cardiovascular disease or end organ damage.
In which patients is the first line medical management of HTN a calcium channel blocker such as amlodopine?
Aged over 55 or black of African or African-Caribbean descent
What is the first line medical management of HTN in patients of non-African or non-African-Caribbean descent who are under 55?
Ace inhibitor (ramipril) or ARB if not tolerated (candesartan)
What is the second line medical management in HTN?
Ace inhibitor (ramipril)/ARB(candesartan) if African or African-Caribbean or if ACEi not tolerated + calcium channel blocker (amlodopine)
OR Calcium channel blocker (amplodopine)+ thiazide like diuretic (indapamide)
OR Ace inhibitor (ramipril)/ARB(candesartan) if African or African-Caribbean or if ACEi not tolerated + thiazide like diuretic (indapamide)
Third line medical management of HTN?
Step 3
ACEi/ARB + Calcium channel blocker + Thiazide-like diuretic
Fourth line medical management in HTN?
If serum K+ less than or equal to 4.5 postassium sparing diuretic (spironolactione)
Otherwise consider alpha blocker (doxazosin) or beta blocker (atenolol)
When should specialist advice be sought when medically managing HTN?
If foruth line management still fails
How do the different diuretics to treat HTN affect serum potassium?
Spironolactone - can cause hyperkalemia (ditto ACEi) as the increase potassium reabsorption
Thiazide diuretics can cause hypokalemia
Mechanism of action of spironolactone?
Aldoserone agonist Competitively blocks androgen receptors Weakly inhibits androgen synthesis Reduced aldosterone Increased sodium excretion, decreased potassium excretion
Mechanism of action - thiazide diuretic?
• Inhibit N+/Cl- co-transporter in distal convoluted tubule
↓Na+ and H2O reabsorption (RAAS compensates with time)
• Long term effects mediated by sensitivity of vascular smooth
muscle to vasoconstrictors Ca2+/NAd
Loss of Na and water, hypokalemic metabolic alkalosis, increase Ca2+ absorption
Mechanism of action - loop diuretic?
Loop diuretics induce its effect by competing with chloride to bind to the Na-K-2Cl (NKCC2) cotransporter at the apical membrane of the thick ascending limb of loop of Henle, reduced Na + reabsorption
HTN treatment targets for <80yrs?
BP<140/90
HTN treatment targets>80 years?
<150/90
How should patients with HTN be advised re:lifestyle
This includes recommending a healthy diet, stopping smoking, reducing alcohol, caffeine and salt intake and taking regular exercise.
What causes S1?
Closing of the atrioventricular valves (tricuspid +mitral) at the start of the systolic contraction of the ventricles
When do the tricuspid and mitral valves close?
Systolic contraction of the ventricles
What causes S2?
Closing of the semilunar valves (pulmonary and aortic valves) once the systolic contraction is complete
Prevents blood flow back from pulmonary arteries or aorta into the ventricles
When do the pulmonary and aortic valves close?
Once systolic contraction is complete
When is S3 heard (if at all)?
0.1 seconds after first heart sound
Rapid ventricular filling causes the chordae tendineae to pull to their full length and twang
Why might S3 be heard in healthy patients aged 15-40?
Heart functions so well the ventricles easily allow rapid filling
chordae tendineae pull to full length and twang
Why might S3 be heard in older patients?
Indicative of HF as the ventricles and chordae are stiff and weak so they reach their limit much faster than normal
Describe s1, s2, and s3?
S1 lub
S2 dub
S3 (lub, de, dub)
When might S4 be heard and what does it indicate?
Directly before S1.
Always abnormal - rare
Indicates a stiff or hypertrophic ventricle
Caused by turbulent flow from an atria contracting against a non-compliant ventricle
Which side of stethoscope should be used to hear low pitched sounds (murmurs)?
Bell
Which side of stethoscope should be used to hear high pitched sounds?
Diaphragm
In terms of ascultation of the chest, where is the pulmonary area?
2nd ICS
Left sternal boarder
In terms of ascultation of the chest, where is the aortic area?
2nd intercostal space
Right sternal boarder
In terms of ascultation of the chest, where is the tricuspid area?
5th ICS
Left sternal boarder
In terms of ascultation of the chest, where is the mitral area?
5th ICS (just below nipple) Midclavicular line
Which point is best for listening to heart sounds?
Erb’s point
Where is Erb’s point?
3rd ICS, left sternal boarder
How should a murmur be described?
SCRIPT
S – Site: where is the murmur loudest?
C – Character: soft / blowing / crescendo (getting louder) / decrescendo (getting quieter) / crescendo-decrescendo (louder then quieter)
R – Radiation: can you hear the murmur over the carotids (AS) or left axilla (MR)?
I – Intensity: what grade is the murmur?
P – Pitch: is it high pitched or low and grumbling? Pitch indicates velocity.
T – Timing: is it systolic or diastolic?
How are cardiac murmurs graded?
1 - Difficult to hear
2 - Quiet
3 - Easy to hear
4 - Easy to hear with a palpable thrill
5 - Can hear with stethoscope barely touching chest
6- Can hear with stethoscope off the chest
If in doubt 2 or 3
What special manouevures can be used to emphasise certain murmurs?
Patient lies on LHS - mitral stenosis
Patient sat up, leaning forward and holding expiration - aortic regurg
What kind of cardiac remodeling can valvular heart disease cause?
Hypertrophy - thickening of myocardium both outwards and into the chamber
Dilation - thinning and expanding of the myocardium
What cardiac remodeling can mitral stenosis cause?
Left atrial hypertrophy
What kind of cardiac remodeling can aortic stenosis cause?
Left ventricular hypertrophy
What valvular disease causes hypertophy?
Stenotic disease Mitral stenosis (left atrial) Aortic stenosis (left ventricular)
What is mitral stenosis?
This is a narrow mitral valve making it difficult for the left atrium to push blood through to the ventricle.
What kind of valvular heart disease can cause dilation?
Regurgatative
Mitral regurgitation causes left atrial dilatation.
Aortic regurgitation causes left ventricular dilatation.
What changes to the heart might mitral regurg cause?
Left atrial dilation
What kind of heart changes might aortic regurg cause?
Left ventricular dilation
What causes mitral stenosis?
Rheumatic heart disease
Infective endocarditis
What murmur is caused by mitral stenosis?
It causes a mid-diastolic, low pitched “rumbling” murmur
(due to a low velocity of blood flow)
There will be a loud S1 due to thick valves requiring a large systolic force to shut, then shutting suddenly.
You can palpate a tapping apex beat due to loud S1.
dub DRrrr
What is mitral stenosis associated with?
Malar flush. This is due to back-pressure of blood into the pulmonary system causing a rise in CO2 and vasodilation.
Atrial fibrillation. This is caused by the left atrium struggling to push blood through the stenotic valve causing strain, electrical disruption and resulting fibrillation.(left atrial strain)
What is mitral regurgitation?
Mitral regurgitation is when an incompetent mitral valve allows blood to lead back through during systolic contraction of the left ventricle.
It results in congestive cardiac failure because the leaking valve causes a reduced ejection fraction and a backlog of blood that is waiting to be pumped through the left side of the heart.
What kind of murmur is heard in mitral regurg?
It causes a pan-systolic, high pitched “whistling” murmur
(due to high velocity blood flow through the leaky valve.)
The murmur radiates to left axilla.
You may hear a third heart sound.
BUUURRRRR
Causes of mitral regurg?
Idiopathic weakening of the valve with age - MOST COMMON
Ischaemic heart disease
Infective Endocarditis
Rheumatic Heart Disease
Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome
What murmurs might be heard in aortic stenosis?
It causes an ejection-systolic, high pitched murmur (high velocity of systole).
This has a crescendo-decrescendo character due to the speed of blood flow across the value during the different periods of systole.
Flow during systole is slowest at the very start and end and fastest in the middle.
Murmur radiates to carotids (as the turbulence continues up into the neck)
BURRR DUB (?VELCRO)
Signs associated with aortic stenosis?
Slow rising pulse and narrow pulse pressure
Patients may complain of exertional syncope (light headedness and fainting when exercising) due to difficulty maintaining good flow of blood to the brain
Causes of aortic stenosis?
Idiopathic age related calcification (MOST COMMOM)
Rheumatic Heart Disease
What kind of murmur is heard in aortic regurg?
Aortic regurgitation typically causes an early diastolic, soft murmur. LUB TARRR
Can also caused ‘Austin Flint’ murmur - this is heard at the apex and is an early diastolic rumbling murmur (caused by blood flowing back through the aortic valve and over the mitral valve causing it to vibrate)
What sign is aortic regurg associated with and why?
A Corrigan’s pulse is also called a collapsing pulse and is a rapidly appearing and disappearing pulse at carotid as the blood is pumped out by the ventricles and then immediately flows back through the aortic valve back into the ventricles.
Causes of aortic regurg?
Idiopathic age related weakness
Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome
How can aortic regurg lead to heart failure?
Aortic regurgitation results in heart failure due to a back pressure of blood waiting to get through the left side of the heart.
Most common valvular disease?
Aortic stenosis is the most common valve disease you will encounter.
It causes an ejection-systolic, high pitched murmur (high velocity of systole).
This has a crescendo-decrescendo character due to the speed of blood flow across the value during the different periods of systole.
Flow during systole is slowest at the very start and end and fastest in the middle.
Where will patients who have had a valve replacement usually have a scar?
Midline sternotomy scar - mitral or aortic valve replacement or CABG)
(Less common - right sided mini-thoracotomy incision used for mitral valve repleacement surgery (minimally invasive)
What are the two main types of prosthetic heart vavev?
Valves can be either replaced by a bioprosthetic or a metallic mechanical valve. “Porcine” bioprosthetic valves come from a pig.
Bioprosthetic valves have a limited lifespan of around 10 years.
Mechanical valves have a good lifespan (well over 20 years) but require lifelong anticoagulation with warfarin. The INR target range with mechanical valves is 2.5 – 3.5.
Pros and cons of mechanical valve?
Good lifespan - over 20 years (vs 10 years for bioprsthetic)
Requires lifelong anticoagulation with warfarin with a targer INR of 2.5-3.5
Target INR for a patient with a mechanical valve?
2.5-3.5
Types of mechanic heart valves?
Starr-Edwards valve
- Ball in cage valve
- Very successful but no longer being implanted
- Highest risk of thrombus formation
Tilting disc valve
-A single tilting disc
St Jude Valve
- Two tilting metal discs
- The two discs mean they are called bileaflet valve
- Least risk of thrombus formation
Major complications of mechanical valves?
Thrombus formation (blood stagnates and clots) Infective endocarditis (infection in prosthesis) Haemolysis causing anaemia (blood gets churned up in the valve)
What will be heard in a patient with a mechanical mitral vavle?
Click in place of S1
What will be heard in a patient with a mechanical aortic valve?
Click in place of S2
What is a Transcatheter Aortic Valve Implantation (TAVI)?
This is a treatment for severe aortic stenosis, usually in patients that are high risk for an open valve replacement operation. It involves local or general anaesthetic, inserting a catheter in to the femoral artery, feeding a wire under xray guidance to the location of their aortic valve, then inflating a balloon to stretch the stenosed aortic valve and implanting a bioprosthetic valve in the location of the aortic valve.
Why is open heart surgery to replace an aortic valve in severe aortic stenosis the first line in younger fitter patients?
Long term outcomes for TAVI are still not clear as it is a relatively new procedure. Therefore in younger, fitter patients open surgery is still the first line option.
Which organisms typically cause endocarditis in patients who have a prosthetic valve?
Gram positive cocci
Staphylococcus
Streptococcus
Enterococcus
What is the pathological process of AF?
Normally the sinoatrial node produces organised electrical activity that coordinates contraction of the atria of the heart.
In AF disorganised electrical activity overrides the SA node, so contraction of the atria is uncoordinated, rapid, and irregular.
This disorganised electrical activity in the atria also leads to irregular conduction of electrical impulses to the ventricles?
What does an absence of P waves indicate on ECG?
Lack of coordinated electrical activity
What problems might AF cause?
Irregularly irregular ventricular contractions - palpitations
Tachycardia
Heart failure due to poor filling of the ventricles during diastole
Risk of stroke
Why can AF cause stroke?
There is a tendency for blood to collect in the atria and form blood clots. These clots can become emboli, travel to the brain and block the cerebral arteries causing an ischaemic stroke.
How might AF present?
Often asymptomatic - incidental finding when pt is attending for other reasons
Palpitations
Shortness of breath
Syncope (dizziness or fainting)
Symptoms of associated conditions (e.g. stroke, sepsis or thyrotoxicosis)
What are the two differential for an irregularly irregular pulse?
Atrial fibrillation
Ventricular ectopics
How can AF and ventricular ectopics be differentiated from AF?
Using an ECG stress test
Ventricular ectopics disappear when the heart rate gets over a certain threshold. Therefore a regular heart rate during exercise suggests a diagnosis of ventricular ectopics.
What is seen on ECG in AF?
Absent P waves
Narrow QRS Complex Tachycardia
Irregularly irregular ventricular rhythm
What is valvular AF?
Valvular AF is defined as patients with AF who also have moderate or severe mitral stenosis or a mechanical heart valve. The assumption is that the valvular pathology itself has lead to the atrial fibrillation.
What is non-valvular AF?
Patients without a prosthetic valve
Patients without:
aortic regurg or aortic stenosis????
Most common AF causes?
SMITH Sepsis Mitral Valve Pathology (stenosis or regurgitation) Ischemic Heart Disease Thyrotoxicosis Hypertension
Principles of treating AF?
Rate or rhythm control
Anticoagulation to prevent stroke
When is rate control the first line management in AF?
Irreversable cause
AF is not new onset (last 48hrs)
AF does not cause HF
When should rhythm control be offered to patients with AF?
There is reversible cause for their AF
Their AF is of new onset (within the last 48 hours)
Their AF is causing heart failure
They remain symptomatic despite being effectively rate controlled
Options for rate control in AF?
Beta blocker is first line (e.g. atenolol 50-100mg once daily)
Calcium-channel blocker (e.g. diltiazem) (not preferable in heart failure)
Digoxin (only in sedentary people, needs monitoring and risk of toxicity)
Why is rate control aimed for in most pts with AF?
Normally the function of the atria is to pump blood in to the ventricles.
In AF atrial contractions are not coordinated so the ventricles have to fill up by suction and gravity. This is considerably less efficient.
The higher the heart rate, the less time is available for the ventricles to fill with blood, reducing the cardiac output.
The aim is to get the heart rate below 100 to extend the time during diastole when the ventricles can fill with blood.
Aim of rhythm control in AF?
The aim of rhythm control is to return the patient to normal sinus rhythm.
This can be achieved through a single “cardioversion” event that puts the patient back in to sinus rhythm or long term medical rhythm control that sustains a normal rhythm.
Patients with AF who are candidates for rhythm control should have cardioversion considered, what are the two types and when is each used?
Immediate cardioversion if the AF has been present for less than 48 hours or they are severely haemodynamically unstable.
Delayed cardioversion if the AF has been present for more than 48 hours and they are stable.
How long before delayed cardioversion should a patient be coagulated for and why? What should they be offered during this period?
Minimum 3 weeks prior
Essential because during the 48 hrs prior to cardiversion they may have developed a clot in the atria and reverting them back to SNR carries a high risk of mobilising the clot and causing a stroke.
The should have rate control whilst waiting for cardioversion (beta blocker/CCB/digoxin)
What are the the two options for cardioversion?
Pharmacological cardioversion
Electrical cardioversion
First line pharmacological cardioversion?
Flecanide Amiodarone (the drug of choice in patients with structural heart disease)
What happens during electrical cadioversion?
The aim of electrical cardioversion is to rapidly shock the heart back into sinus rhythm.
This involves sedation or a general anaesthetic and using a cardiac defibrillator machine to deliver controlled shocks in an attempt to restore sinus rhythm.
Long term medical rhythm control for AF includes what?
Beta blockers are first line for rhythm control
Dronedarone is second line for maintaining normal rhythm where patients have had successful cardioversion
Amiodarone is useful in patients with heart failure or left ventricular dysfunction
What is paroxysmal AF?
Paroxysmal AF is when the AF comes and goes in episodes, usually not lasting more than 48 hours.
Management of paroxysmal AF?
Anti-coagulated based on CHADVASc score
Pill in pocket - PRN to terminate AF only when they feel symptoms starting ONLY APROPRIATE IN PATIENTS WITHOUT UNDERLYING STRUCTUAL DISEASE they must also be able to understand when they are in AF and understand when treatment is appropriate - FLECANIDE is the usual treatment
When should flecanide be avoided and why?
Avoid flecanide in atrial flutter as it can cause 1:1 AV conduction and resulting in a significant tachycardia.
What is the HAS-BLED score and why does it carry less weight than CHADVASc?
Risk of a serious bleed each year for patients on anticoagulation
Generally bleeds are more reversible than strokes and have less long term consequences.
How does Warfarin anticoagulate?
Warfarin is a vitamin K antagonist.
Vitamin K is essential for the functioning of several clotting factors and warfarin blocks vitamin K (Clotting factors dependent on vitamin K include factor II, which is prothrombin, factor VII, factor IX and factor X )
It prolongs the prothrombin time, which is the time it takes for blood to clot.
What clotting factors are Vit K dependent?
Factor II, which is prothrombin,
Factor VII,
Factor IX
Factor X
How do we assess how anticoagulated a pt on warfarin is?
INR - international normalised ratio
What is INR?
The INR is a calculation of how the prothrombin time of the patient compares with the prothrombin time of a normal health adult. An INR of 1 indicates a normal prothrombin time. An INR of 2 indicates that the patient has a prothrombin time twice that of a normal healthy adult (it takes them twice as long to form a blood clot).
Target INR for pts on warfarin with AF?
The target INR for AF is 2 – 3.
Which system in the body is involved in the metabolism of warfarin?
cytochrome P450 system in the liver
What might influence the activity of warfarin?
Drugs that influence the activity of the P450 system in the liver
Foods high in Vit K - leafy green vegetables
Drinks which affect P450 - cranberry juice, alaochol
Half life of warfarin? How can it quickly be reversed?
Warfarin has a half-life of 1-3 days. It is also reversible with vitamin K in the event that the INR is very high or bleeding has occurred.
How often should DOACs be taken?
Apixaban and dabigatran are taken twice daily, rivaroxaban is taken once daily.
How often should DOACs be taken?
Apixaban and dabigatran are taken twice daily, rivaroxaban is taken once daily.
What reversal agent is used when a patient on DOACs has a life threatening bleed?
Andexanet alfa (apixaban and rivaroxaban) Idarucizumab (a monoclonal antibody against dabigatran)
Which antibiotic interacts with warfarin to cause an increased INR?
Fluoroquinolones may increase INR by inhibiting warfarin metabolism, displacing warfarin from protein-binding sites, or disturbing intestinal flora that synthesizes vitamin K. (ciprofloxacin)
Contraindications against warfarin?
Malignancy (heparin or a DOAC must be used in this instance)
Known hypersensitivity to warfarin or its ingredients
Haemorrhagic stroke
Clinically significant bleeding
Potential bleeding lesions (e.g. active peptic ulcer, oesophageal varices)
Uncorrected major bleeding diathesis (e.g. haemophilia, chronic kidney disease)
Pregnancy, due to the risk of congenital malformations and fetal death (breastfeeding is allowed)
Within 72 hours of major surgery with the risk of severe bleeding
Within 48 hours postpartum
Uncontrolled severe hypertension
Patient factors (e.g. uncooperative, unreliable and/or high risk of repeated falls)
Drugs with which there is a significantly increased risk of bleeding (e.g. antiplatelet drugs*, non-steroidal anti-inflammatory drugs, and enzyme inhibitors)
After how long does warfarin achieve an INR within the therapeutic range?
up to five days to achieve an INR within the therapeutic range
Examples of P450 inducers that will decrease INR when given alongside warfarin?
Enzyme inducers decrease the amount of active warfarin in the body and thus decrease its efficacy (decrease INR). These include alcohol, allopurinol, paracetamol, SSRIs, lipid-regulating drugs, influenza vaccine.7
Examples of P450 inhibitors that will increase INR when given alongside warfarin?
Enzyme inhibitors increase the amount of active warfarin in the body and thus increase its potency (increase INR). These include oral contraceptives and St John’s wort.7
How is CHA2DS2-VASc scored?
C – Congestive heart failure H – Hypertension A2 – Age >75 (Scores 2) D – Diabetes S2 – Stroke or TIA previously (Scores 2) V – Vascular disease A – Age 65-74 S – Sex (female)
What tool is now used to assess a patient’s risk of bleeding on anticoagulation and what does it score based on?
ORBIT
Low haemoglobin or haematocrit Age (75 or above) Previous bleeding (gastrointestinal or intracranial) Renal function (GFR less than 60) Antiplatelet medications
What causes a cardiac arrhythmia?
interruption to the normal electrical signals that coordinate the contraction of the heart muscle
What are the cardiac arrest (pulesless unresponsible patient) rhythms that might be seen?
Shockable: VT, VF (defib can be used)
Non-shockable: Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
Asystole (no significant electrical activity) (defib should not be used)
How should a pt with tachycardia who is unstable be treated?
Consider up to 3 synchronised shocks
Consider an amiodarone infusion
Causes and management of narrow complect tachycardia (assuming pt is stable)?
Narrow complex (QRS < 0.12s)
Atrial fibrillation – rate control with a beta blocker or diltiazem (calcium channel blocker)
Atrial flutter – control rate with a beta blocker
Supraventricular tachycardias – treat with vagal manoeuvres and adenosine
Causes and management of broad complex tachycardia (assuming pt is stable)?
Broad complex (QRS > 0.12s)
Ventricular tachycardia or unclear – amiodarone infusion
If known SVT with bundle branch block treat as normal SVT - vagal manouever + adenosine
If irregular may be AF variation – seek expert help
What constitutes a narrow complex tachycardia?
QRS less than 0.12s
What constitutes a broad complex tachycardia?
QRS more that 0.12s
When a patient has no pulse and is unresponsive, what are the only two rhythms that can be shocked?
Ventricular tachycardia
Ventricular fibrillation
Pathophysiology of atrial flutter?
Normally the electrical signal passes through the atria once, simulating a contraction then disappears through the AV node into the ventricles
In atrial flutter there is a ‘re-entrant rhythm in either atrium
Electrical signal re-circulates in a self perpetuating loop due to an extra electrical pathway
The signal goes round and round the atrium without interruption
This stimulates atrial contraction at 300bpm
This signal makes its way into the ventricles every second lap due to the long refractory period to the AV nodes, causing a 150bpm ventricular contraction
Atrial flutter as seen on ECG?
It gives a “sawtooth appearance” on ECG with P wave after P wave.
Conditions associated with atrial flutter?
Associated Conditions:
Hypertension
Ischaemic heart disease
Cardiomyopathy
Thyrotoxicosis
How is atrial flutter treated?
Rate/rhythm control with beta blockers or cardioversion - DO NOT USE FLECANIDE
Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
Radiofrequency ablation of the re-entrant rhythm
Anticoagulation based on CHA2DS2VASc score
What causes and SVT?
Supraventricular tachycardia (SVT) is caused by the electrical signal re-entering the atria from the ventricles. Normally the electrical signal in the heart can only go from the atria to the ventricles. In SVT the electrical signal finds a way from the ventricles back into the atria. Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction. This causes a self-perpetuating electrical loop without an end point and results in fast narrow complex tachycardia (QRS < 0.12).
How is SVT seen on ECG?
fast narrow complex tachycardia (QRS < 0.12). It looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.
What is paroxysmal SVT?
Paroxysmal SVT describes a situation where SVT reoccurs and remits in the same patient over time.
What are the three main types of SVT?
Classified by source of electrical signal
- Atrioventricular nodal re-entrant tachycardia
- Atrioventricular re-entrant tachycardia
- Atrial tachycardia
What is atrioventricular nodal re-entrant tachycardia?
“Atrioventricular nodal re-entrant tachycardia” is SVT when the re-entry point is back through the AV node.
What is Atrioventricular re-entrant tachycardia?
SVT where the re-entry point is an accessory pathway (e.g. WPW)
What is atrial tachycardia?
SVT where the electrical signal orginates in the atria somewhere other than the sinoatrial node.
What causes atrial tachycardia?
This is not caused by a signal re-entering from the ventricles but instead from abnormally generated electrical activity in the atria. This ectopic electrical activity causes an atrial rate of >100bpm.
Acute management of a stable patient with SVT?
- Put patient on continuous ECG mointoring and then adopt a stepwise approach
1. Valsalva manoeuvre. Ask the patient to blow hard against resistance, for example into a plastic syringe.
2. Carotid sinus massage - massage carotid on one side gently with two fingers
3. Adenosine - 6mg then 12mg and a further 12mg if no improvement between doses OR VERAPIMIL if contraindicated
D4. Direct current cardioversion if above fails
How does adenosine treat SVT?
Slows cardiac conduction through the AV node
Interrupting of AV node/acessory pathway during SVT and resets to SR
Needs to be given as a rapid blus to ensure it reaches the heart with enough impact to interrupt the pathway
Causes brief asystole or bradycardia - warn patients they may experience sensation of impending doom
How should adenosine be given in acute SVT?
Give as a fast IV bolus into a large proximal cannula (e.g. grey cannula in the antecubital fossa)
When should adenosine be avoided?
Asthma COPD HF Heart block Severe hypotension
Long Term Management of patients with paroxysmal SVT?
Medication (beta blockers, calcium channel blockers or amiodarone)
Radiofrequency ablation
What is WPW syndrome caused by?
Atrioventricular re-entrant tachycardia - extra electrical pathway connects the atria and ventricles - often called Bundle of Kent
What is the definitive treatment for Wolff-Parkinson White syndrome?
Radiofrequency ablation of the accessory pathway
ECG changes in WPW?
Short PR interval (< 0.12 seconds)
Wide QRS complex (> 0.12 seconds)
“Delta wave” which is a slurred upstroke on the QRS complex
If the person has a combination of atrial fibrillation or atrial flutter and WPW what is there an addition risk of?
The chaotic atrial electrical activity can pass through the accessory pathway into the ventricles
This can cause a polymorphic wide complex tachycardia
Most antiarrythmic medications increase the risk of this by reducing conduction through the AV node, so therefore beta blockers, calcium channel blockers, adenosine etc are contraindicated in patients with WPW who develop AF/atrial flutter
What does radiofrequency ablation involve?
Catheter ablation is performed in a “cath lab”.
It involves local or general anaesthetic, inserting a catheter in to the femoral veins and feeding a wire through the venous system under xray guidance to the heart.
Once in the heart it is placed against different areas to test the electrical signals at that point. This way the operator can hopefully find the location of any abnormal electrical pathways.
The operator may try to induce the arrhythmia to make the abnormal pathways easier to find.
Once identified, radiofrequency ablation (heat) is applied to burn the abnormal area of electrical activity. This leaves scar tissue that does not conduct the electrical activity. The aim is to remove the source of the arrhythmia.
RFA can be curative for certain cases of arrhythmia caused by abnormal electrical pathways, including what?
Atrial Fibrillation
Atrial Flutter
Supraventricular Tachycardias
Wolff-Parkinson-White Syndrome
What is torsades de pointes?
Polymorphic VT
VT on ECG with QRS complec twisting around the baseline, progressively getting smaller and then larger in height and then smaller and so on
When does Torsades de pointes occur?
Prolonged QT interval
Normal QTc interval?
<450 milliseconds (ms) for men and <460 ms for women
Pathophysiology of Torsades de pointes?
Prolonged repolarisation of the muscle cells in the heart after a contraction
Results in random, spontaneous depolarisation in some areas of heart myocytes (afterdepolarisations)
These spread throughout the ventricle leading to a ventricular contraction prior to proper repolarisation occuring
The ventricles continue to stimulate recurrent contractions without normal repolorisation
What is cardiac depolorisation?
Depolarisation is the electrical process that leads to the heart contraction.
What is cardiac repolorisation?
Repolarisation is a period of recovery before the heart muscle cells (myocytes) are ready to depolarise again.
What happens when a patient develops Torsades de pointes?
When a patient develops Torsades de pointes it will either terminate spontaneously and revert back to sinus rhythm or progress in to ventricular tachycardia. Usually they are self limiting but if they progress to VT it can lead to a cardiac arrest.
Causes of prolonged QT?
Long QT Syndrome (inherited)
Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)
Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)
Acute Management of Torsades de pointes
Correct the cause (electrolyte disturbances or medications)
Magnesium infusion (even if they have a normal serum magnesium)
Defibrillation if VT occurs
How is Prolonged QT syndrome managed long term?
Avoid medications that prolong the QT interval Correct electrolyte disturbances Beta blockers (not sotalol) Pacemaker or implantable defibrillator
What is a ventricular ectopic?
Ventricular ectopics are premature ventricular beats caused by random electrical discharges from outside the atria.
What might patients complain of if they are having ventricular ectopics?
Random, brief, palpitations
Who is affected by ventricular ectopics?
They are relatively common at all ages and in healthy patients however they are more common in patients with pre-existing heart conditions (e.g. ischaemic heart disease or heart failure).
How might venticular ectopics appear on ECG?
They can be diagnosed by ECG and appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG.
What is Bigeminy?
This is where the ventricular ectopics are occurring so frequently that they happen after every sinus beat. The ECG looks like a normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic and so on.
How are otherwise healthy people with ventricular ectopics managed?
Reassurance, no treatment
In a patient having ventricular ectopics what else should you investigate for?
Anaemia
Electrolyte disturbance
Thyroid abnormalities
Under what circumstances would you seek expert advice in a patient suffering from ventricular ectopics?
Background of heart conditions Chest pain Syncope Murmur Fhx sudden death
What is first degree AV Node block? What is seen on ECG?
First-degree heart block occurs where there is delayed atrioventricular conduction through the AV node.
Despite this, every atrial impulse leads to a ventricular contraction, meaning every p waves results in a QRS complex.
On an ECG this presents as a PR interval greater than 0.20 seconds (5 small or 1 big square).
What is second-degree heart block?
Second-degree heart block is where some of the atrial impulses do not make it through the AV node to the ventricles. This means that there are instances where p waves do not lead to QRS complexes.
(There are several patterns of this)
What happens in Wenkebach’s phenomenon (Mobitz type 1) and what ECG changes are seen?
This is where the atrial imputes becomes gradually weaker until it does not pass through the AV node. After failing to stimulate a ventricular contraction the atrial impulse returns to being strong. This cycle then repeats.
On an ECG this will show up as an increasing PR interval until the P wave no longer conducts to ventricles. This culminates in absent QRS complex after a P wave. The PR interval then returns to normal but progressively becomes longer again until another QRS complex is missed. This cycle repeats itself.
What happens in Mobitz Type 2 and what ECG changes are seen?
This is where there is intermitted failure or interruption of AV conduction. This results in missing QRS complexes. There is usually a set ratio of P waves to QRS complexes, for example 3 P waves to each QRS complex would be referred to as a 3:1 block. The PR interval remains normal.
What is an important risk of Mobitz type 2 that isn’t also associated with Mobitz type 1?
Asystole
What is meant by 2:1 block on ECG and what causes it?
This is where there are 2 P waves for each QRS complex. Every second p wave is not a strong enough atrial impulse to stimulate a QRS complex.
It can be caused by Mobitz Type 1 or Mobitz Type 2 and it is difficult to tell which.
What is Third degree heartblock?
This is referred to as complete heart block.
This is no observable relationship between P waves and QRS complexes.
There is a significant risk of asystole with third-degree heart block.
When is a patient with AV Node block at risk of asystole?
Mobitz type 2
Complete heart block
Previous asytole
How should a stable patient with first degree or Mobitz Type 1 heartblock be managed?
Observation only
How should patients with heart block considered unstable or at risk of asystole be managed?
1st Line, Atropine - 500mcg IV - if no improvement
- Atropine 500mcg IV repeated up to 6 doses (total 3mg)
- Use of other inotropes such as noradreniline
- Transcutaneous cardiac pacing (using a defib)
What should be done for patients with a high risk of asystole?
Temporary transvenous cardiac pacing
Permanent implantable pacemaker when available
How is transvenous cardiac placing undertaken?
Using an electrode on the end of a wire that is inserted into a vein and fed through the venous system to the right atrium or ventricle to stimulate them directly
Atropine use leads to side effects of pupil dilatation, urinary retention, dry eyes and constipation - why?
Antimuscarinic medication that works by inhibiting the parasympathetic nervous system
What do artifical pacemakers consist of?
Pule generator Pacing leads (carry electrical impulses to the relevant part of the heart
What is the role of an artificial pacemaker?
Delivers controlled electrical impulses to specific areas of the heart to restore the normal electrical acitivity and improve the heart function
How is a pacemaker inserted?
The box is implanted under the skin (most commonly in the left anterior chest wall or axilla) and the wires are implanted into the relevant chambers of the heart.
What might pacemakers (especially older ones) be a contraindication for?
MRI scans (due to powerful magnets) and electrical interventions such as TENS machines and diathermy in surgery
How long do pacemaker batteries last?
5 years
Indications for a pacemaker?
- Symptomatic bradycardias
- Mobitz Type 2 AV block
- Third degree heart block
- Severe heart failure (biventricular pacemakers)
- Hypertrophic obstructive cardiomyopathy (ICDs)
What are the types of pacemaker?
Single chamber pacemaker (leads in either right atrium OR right ventricle)
Dual chamber pacemaker (lead in right atrium and right ventricle)
Biventricular (triple-chamber pacemaker) (leads in right atrium, right ventricle and left ventricle)
Implantable Cardioverter Defibrillators (ICDs)
When is a single-chamber pacemkaer placed in the right atrium and how does it act?
Patient has normal AV conduction
Issue is with SA node
Stimulates depolarisation in right atrium and this electrical activity passes to the left atrium through the AV node to the ventricles in the normal way
When is a single-chamber pacemkaer placed in the right ventricle and how does it act?
If the patient has abnormal AV conduction
Stimulates the ventricles directly (ie. not via AV node as it would if placed in right atrium)
What does a dual chamber pacemaker allow?
Synchronisation of the contractions of both atria and ventricles
When is a biventricular pacemaker used and what is the objective of it?
In patients with heart failure
Objective to synchronise the contractions in these chambers to try and optomise the heart function
(Also known as cardiac resynchronisation therapy (CRT) pacemaker)
What does an Implantable cardioverter defibrilator do?
Continually monitors the heart and applies a defibrillator shock to cardiovert the patient back into sinus rhythm if it identifies a shockable arrythmia
How can a pacemaker intervEnetion be seen on ECG?
Sharp vertical line on all leads
Where will the vertical line appear on ECG for a single-chamber pacemaker?
Before either the P OR QRS
Where will the vertical line appear on ECG for a dual-chamber pacemaker?
Line before BOTH P and QRS
Biomarkers for MI?
hs-TnI will frequently be > 100 ng/L (and
CK usually > 400)
When will troponin be raised in patients with an MI?
TnI levels begin to rise 3 to 4 hours after myocardial damage and stay elevated for up to two
weeks. CK should also be measured in STEMI patients.
How can hs-TnI be used in patients with suspected MI?
In order to achieve a quick diagnosis we recommend a hs-TnI level is taken on admission
and again at 1 hour. Only one hs-TnI level is required if the onset of symptoms was 3 or
more hours previously. If there is uncertainty, a further sample can be taken a further 2
hours later (3 hours after the first). Second hs-TnI levels can be useful to assess whether the
elevation is static, rising or falling.
What long term condition most commonly causes a false positive increase in hs-TnI?
Advanced renal failure
When should ST depression without any ST elevation or new left bundle branch block still be suspicious of a stemi?
ST depression confined to leads V1 to V4 may have true posterior myocardial infarction and
should be treated in the same manner as STEMI.
ST elevation in RV4 is highly sensitive for what?
Right ventricular infarction
How should ECG changes not attriubtable to a current STEMI be considered?
In the case of unstable angina and NSTEMI the ECG changes may manifest as transient ST
segment depression or elevation, T wave inversion or flattening, T wave pseudo normalisation (or even no change at all).
Previously established ECG changes such as old MI,
LV hypertrophy and digoxin effect need to be considered.
What might mimic a STEMI on ECG?
- Early repolarisation can cause up-sloping ST elevation, particularly in V1 and V2 (sometimes V3). It is more commonly seen in younger patients who are athletics, and some afro-caribbean patients.
- There my be concave ST elevation in pericarditis and the ST changes may be very widespread.
- Burgada syndrome may also be misdiagnosed as an anterior STEMI.
- Takotsubo cardiomypoathy (stress reaction mostly middle aged females) can mimic STEMI and NSTEMI
What is Brugada syndrome?
A genetic disorder characterised by a disruption in the normal heart rhythm. The common symptom is fainting.
What is Takotsubo cardiomyopathy?
'’broken heart syndrome’’
A temporary condition in which there is a sudden enlargement of the heart muscles, usually caused due to extreme emotional or physical stress.
What, in terms of physiological cause, is the difference between STEMI and NSTEMI?
STEMI - complete occlusion of the coronary artery
NSTEMI - partial occlusion of the coronary artery
When there is uncertainty of diagnosis of NSTEMI, what can be done?
A bedside echo looking for regional wall motion
abnormalities (RWMAs) can help the decision
How should Prasugrel be administered in STEMI management?
Prasugrel (thienopyridine inhibits ADP receptors 60 mg loading and 10 mg daily for
up to 12 months, use is restricted to patients undergoing primary percutaneous
coronary intervention (PPCI) for STEMI who are under the age of 75 and who weigh
more than 60kg and who have not had a prior TIA or stroke.
When should clopidogrel be used in MI management?
Patients who do not fufil the criteria for Prasugrel, ie. any of the below
- Over the age of 75
- Weigh less than 60kg
- Previous TIA or storke
- Not undergoing PPCI
How and when is Ticafrelor used in patients having an MI?
Ticagrelor (non thienopyridine loading dose 180mg followed by 90mg bd for up to 12
months, used in patients who cannot have Prasugrel or as first choice NSTEMI)
Dosage of clopidogrel in MI?
Clopidogrel (inhibits ADP receptors, loading dose 600 mg followed by 75mg od for up to 12 months
What bloods MUST be performed in suspected or confirmed MI?
All patients should have a full biochemical screen on admission including lipid profile,
random glucose and an HbA1c assay performed. A full blood count is mandatory.
(+ trop I and CK)
What life long medications are indicated post MI?
Bisoprolol (beta-blocker, reduce heart rate, avoid in shock or
hypotension, starting dose 1.25mg od). Ace inhibitors (prevent muscle overdamage). Ramipril starting dose 2.5 mg od with checking of renal function) OR
Angiotensin receptor blockers (losartan 25mg od starting dose and check renal
function). Uptitrate to maximally tolerated dose.
Statin (such as atorvastatin 80 mg od, target is to reduce LDL-C < 1·8 mmol/L or a 40% reduction in non-HDL-C. Total
cholesterol target should ideally be < 4·0 mmol/L). Consider rosuvastatin 5mg if sensitive to atorvastatin. Ezetemibe if all statins caused side effects
Aspirin 75mg OD
For how long, at least, should a patient be on LMWH after an NSTEMI?
Enoxaparin for 48 hrs based on weight and
creatinine
When should ticagrelor be given post NSTEMI/in unstable angina?
Ticagrelor if risk > 3% (medium) 180mg loading and 90mg BD
if not contraindicated
If a patient with NSTEMI/Unstable angina is awaiting angiography, what anti-anginal medications should be considered?
nitrates, ranolazine,
calcium channel blockers
Differential for stable angina?
Exertional breathlessness
GORD
MSK discomfort
Pulmonary disease
When is chest discomfort likely to represent coronary artery disease (ie. stable angina) as opposed to an MSK, GI or pulmonary complaint?
Two or more of the follwoing: Cigarette smoking, HTN DM, Hypercholesterolaemia Family hx of premature coronary artery disease, or prescence of other aquired vascular disease
What other cardiac conditions may cause angina-like symptoms in the absence of coronary artery disease?
Aortic stenosis, HTN heart disease, hypertrophic cardiomyopathy
What features from the history of a patient with ?stable angina make stable angina less likely?
Angina is unlikely if the pain is continuous or very prolonged, unrelated to activity, brought
on by breathing or associated with other symptoms such as dizziness and dysphagia.
What should be looked for in particular on examination of a patient when ?stable angina is being considered?
• weight and height (to allow calculation of BMI) or waist / hip ratio
• blood pressure
● presence of murmurs, especially that of aortic stenosis
• evidence of hyperlipidaemia
• evidence of peripheral vascular disease and carotid bruits (especially in diabetes).
What should be offered to patients with an estimated likelihood of CAD 61-90%?
Invasive coronary angiography
What should be offered to patients with an estimated likelihood of CAD 30-60% what should be offerend?
Offer functional imaging as the first line diagnostic investigation:
Stress MRI
Echo or myoview
What should be offered to patients with an estimated likelihood of CAD 10-29% what should be offered?
Offer CT calcium scoring as the first line diagnostic investigation (Ct scan measure calcium level)
What should be interperated and actioned from CT calcium scoring?
0 - very minimal likelihood of significant coronary disease
If the score is 1-400 consideration should be given to CTCA or stress perfusion imaging
Above 400, coronary angiography should be seriously considered if appropriate
When should exercise ECG NOT be used to diagnose or exclude stable angina?
In patients without known CAD
Aspirin 75mg OD is used in prevention of CVD, what should be used instead if contraindicated?
Clopidogrel 75mg OD
Rae limitation should be the goal in patients with stable angina with a normal chronotropic response to exercise, how?
This is best achieved with β-blockers and non-dihydropyridine calcium channel
blockers (diltiazem or verapamil).
Ivabradine 5-75mg BD is sometimes used in patients with angina, what is it and when is it used?
a sinus node blocking agent which may be an alternative rate
controlling agent especially where a β-blocker is contra-indicated or not tolerated.
Not to be initiated in angina if heart rate is below 70 bpm. It can be used safely in patients with
impaired LV function. Latest advice is that it should NOT be co-prescribed with diltiazem or
verapamil.
What is Ranolazine (275mg BD up to 750mg BD) used to treat angina?
Ranolazine is licensed as adjunctive therapy in patients who are inadequately controlled or intolerant of first-line anti-anginal drugs.
The dose is initially 375 mg BD increasing to a maximum of 750 mg BD.
Its use should be mainly in patients with chronic stable angina
rather than in the acute setting. Initiation of the drug should be by consultants only.
It is contraindicated if the GFR is < 30.
Main causes of non cardiac chest pain?
- Costochondritis
- Gastro-oesophageal
- PE
- Pneumonia
- Pneumothorax
- Psychogenic/psychosomatic
HTN is usually asymptomatic - if this is not the case then what symptoms may be experienced?
- Headache
- Sweating, headache, palpiations and anxiety (may point to a phaeochromcytoma)
- Muscle weakness or tetany (may point to hyperaldosteronism?)
What family history is important to ascertain in a pt with HTN?
Family history should look for hypertension, premature coronary disease and polycystic
kidney disease
In terms of physical assessment of a patient, what should be looked for in a pt with new HTN?
Look for secondary causes: Cushing’s syndrome, enlarged kidneys (PCK disease), renal
bruits, radio-femoral delay (coarctation).
What investigations should be carried out in a pt. with new HTN?
- Test for the presence of protein in the urine by sending a urine sample for estimation of
the albumin: creatinine ratio and test for haematuria using a reagent strip. - Blood sample to measure plasma glucose, electrolytes, creatinine, estimated glomerular
filtration rate, serum total cholesterol and HDL cholesterol. - Bloods may suggest secondary cause (low potassium, high Na: hyperaldosteronism).
- Examine the fundi for the presence of hypertensive retinopathy.
- Arrange for a 12-lead electrocardiograph to be performed.
- Consider echocardiography if suggestion of LVH, valve disease or LVSD or diastolic dysfunction.
Treatment is always offered in patients with stage 2 or higher HTN, but when is it offered in patients with stage 1?
Pts under 80 plus one of
- Evidence of target organ damage
- Established CVD
- Renal impairment
- Diabetes
- Patients with a Q risk of over 20%
What is a hypertensive crisis?
Increase in blood pressure, which if sustained over matter of hours will lead to irreversable end-organ damaged
What is meant by end-organ damage?
For example Encephalopathy LV failure Aortic dissection Unstable angina Renal failure
How might patients present in HTN emergency?
High BP associated with a critical event: Encephalopathy Pulmonary odema AKI MI
How might hypertensive urgency present?
Malignant HTN Retinal changes (grade 3/4 hypertensive retinopathy)
Aim of therapy in Hypertensive emergency?
Reduce diastolic BP to 110 mmHg in 3-12 hours
Aim of therapy in hypertensive urgency?
Reduce diastolic BP to 110 mmHg in 24 hours
And 100 over 48-72 hours using oral regime
Hypertensive urgency vs hypertensive emergency?
High BP with critical event - emergency
High BP without critical illness - urgency
How is hypertensive crisis managed?
IV to start
1. Sodium nitroprusside
2. Labetalol
3. GTN (1 - 10 mg/hr)
4. Esmolol acts within 60 seconds, with a duration of action of 10 - 20 minutes.
Typically, the drug is given as a 0·5 - 1 mg/kg loading dose over 1 minute, followed by
an infusion starting at 50 µg/kg/min and increasing up to 300 µg/kg/min as
necessary.
How is hypertensive urgency managed in 42-72 hours?
Oral regime Any of: Amlodipine - 5-10mg OD Diltiazem - 120-130mg OD Lisinopril 5mg OD
Most patients will have nifedipine 20mg MR BD plus amlodipine 10mg OD for three days, continuing with amlodipine 10mg OD thereadter
Sustained or paroxysmal hypertension is the most common sign of what endocrine disorder?
Phaochromocytoma
Phaeochromocytoma is treated by tumour resection, but how should HTN be treated in these patients whilst they await surgery?
Combined alpha- and beta-adrenergic blockade
- Phenoxybenzamine most commonly used - If not tolerated, the calcium channel blocker nicardipine can be used.
NEVER use beta-blockers first, used alpha blocker first. Beta blocker is started once alpha blockade is achieved, typically 2-3 days post op
Causes of heart failure?
- Ischaemic heart Disease (most common)
- Hypertension
- Valvular heart disease (Rheumatic fever in elderly)
- Atrial fibrillation
- Chronic lung disease
- Cardiomyopathy (Hypertrophic, dilated and right ventricular, post viral, post-partum)
- Previous cancer chemo drugs
- HIV
How many patients have heart failure with normal eject fraction?
50% - echo will suggest normal systolic function to mild impairment
Similar clinical course outcome as patients with LV systolic dysfunction
Pathophysiology behind HFNEF?
It is hypothesised that the physiology
behind HFNEF relates to impaired filling or diastolic dysfunction
What investigations can be carried out when ?HF
- Renal function (baseline and for diuretic effect),
- FBC (anaemia should be treated as consequence of bone marrow issue)
- LFT’s hepatic congestion
- TFT’s Thyroid disease
- Ferritin and transferrin (Younger patients with possible haemochromatosis)
- Brain natriuretic peptide (NT-proBNP)
Causes of raised NT-proBNP other than heart failure?
Any stimulus which causes increased cardiac chambre stress:
AF
RV strain
6 signs of HF on CXR?
- Cardiomegaly
- Could be pleural effusions
- Perihilar shadowing/consolidations
- Alveolar oedema
- Air bronchograms
- Increased width of vascular pedicle
Possible findings on echocardiogram in HF?
Dilated poorly contracting left ventricle (systolic dysfunction)
Stiff, poorly relaxing, (smaller diameter) left ventricle (diastolic dysfunction);
Valvular heart disease
Atrial myxoma
Pericardial disease
What might be missed on ECHO when investigating HF that will be seen on cardiac MRI?
May miss right ventricle.
Also useful for scar estimation
How are nitrates useful in some patients with HF?
Reduce preload; reduce pulmonary oedema and reduce ventricular size. There is a beneficial effect of using IV nitrates in acute heart failure if there is underlying ischaemia, hypertension or regurgitant aortic and mitral valve disease.
In chronic heart failure they can be especially useful for relief of orthopnoea and exertional dyspnoea
When should caution be applied when using nitrates?
Aortic and mitral stenosis
HOCM
Pericardial constriction
Most common valvular disease?
Aortic stenosis
Three classical symptoms in aortic stenosis?
Angina, HF, syncope
What congenital defect can cause AS?
Congenital bicuspid valve
When is surgery indicated in patients with aortic stenosis?
- If patient is at all symptomatic
Or, asymptomatic with one of the following: - Left ventricular systolic dysfunction
- Abnormal exercise test (symptoms, drop in BP, T changes)
- At time of other cardiac surgery (e.g. CABG)
What are the indications for surgery in chronic aortic regurg?
● Symptomatic severe AR
● Asymptomatic severe AR with evidence of early LV systolic dysfunction (EF < 50% or LV
end-systolic diameter > 5 cm or LV end-diastolic diameter > 7·0 cm)
● Asymptomatic AR of any severity with aortic root dilatation > 5·5 cm (or > 4·5 cm in
Marfan syndrome or bicuspid aortic valve).
What is De Musset’s sign?
Head bobbing
Seen in AR
Most common congenital cause of AR?
Bicuspid valves
AR often has an asymptomatic onset, but it can lead to HF - how?
Patients with chronic aortic regurgitation (AR) may remain asymptomatic for many years despite significant regurgitation.
The increased volume load on the left ventricle leads to
progressive LV dilatation and ultimately heart failure.
Average interval from diagnosis to onset of symptoms in mitral regurg?
16 years
Mitral valve prolapse is one aetiology of mitral regurg, which patients is it more common in?
Marfan’s syndrome
Pectus excavatum
When might MR be acute and severe?
ruptured chordae
ruptured papillary muscle
infective endocarditis
Most patients with MR have mild-moderate disease and never require surgery. When would surgery be indicated?
● Symptomatic patients (with symptoms due to the MR).
● Asymptomatic patients with mild-moderate LV dysfunction (EF 30 - 60% and LVESD 4·5 -5·5 cm)
Medical therapy for MR?
Diuretics
(ACEi only useful in functional or ischemic MR)
(If LV systolic dysfunction present, ACEi, B blockers and CRT)
Predisposing cardiac conditions for infective endocarditis?
mitral valve prolapse
the presence of prosthetic material (e.g. valves and patches, but not coronary stents),
rheumatic heart disease,
degenerative and bicuspid aortic valve disease
congenital heart disease
Most common cause of IE in IVDU?
Staphylococcus aureus
IE occuring up to a year after implantation of prosthetic valves is most commonly caused by what organisims?
Perioperative contamination - stahylococci (especially coagulase-negative)
IE occuring over a year after implantation of prosthetic valves is most commonly caused by what organisims?
Viridans streptococci
Staphylococcus aureus
Coagulase negative staphylococci
What should enterococcal endocarditis be a pointer to?
Disease of GU or lower GI tract
Mortality associated with different aetiologies of infective endocarditis?
Viridans streptococci lower
Staphylococcus aureus higher
Fungal infections highest
Routine investigations for IE?
● Full blood count ● ESR and CRP ● U&Es ● Liver function tests ● Urine dipstick analysis and MSU for microscopy/culture ● Chest X-ray ● ECG ● However, the key diagnostic investigations are: BLOOD CULTURES & ECHOCARDIOGRAM
When should infective endocarditis be suspected?
IE should always be suspected in patients with unexplained fever, bacteraemia or systemic illness and/or with an apparently new murmur or other features of the illness.
How should blood cultures be taken in suspect IE?
x3 sets from different sites over several hours
Reasonable to delay abx treatment if pt stable for comprehensive sampling
What type of echocardiogram is best for detecting vegitations?
Transoesophageal echocardiography - particullary useful for mitral valve and prosthetic valve vegetations
Also more sensitive at detecting aortic root and septal abscesses and leaflet perforations
Treatment of endocarditis caused by streptococci?
Viridans streptococci: benzylpenicillin IV (or vancomycin if penicillin-allergic) plus lowdose gentamicin (e.g. 80 mg BD)
Treatment for endocarditis caused by enterococci?
Enterococcus faecalis: amoxicillin IV (or vancomycin if penicillin-allergic) plus low-dose gentamicin IV (e.g. 80 mg BD)
Treatment of endocarditis caused by staphylococci?
Staph. aureus, Staph. Epidermidis: flucloxacillin (or benzylpenicillin if penicillin-sensitive,
or vancomycin if penicillin allergic or MRSA) plus gentamicin (or fusidic acid)
How is response to therapy monitored in infective endocarditis?
- Echocardiogram (once weekly) - to assess vegetation size and look for complications
(e.g. valve destruction, intracardiac abscesses) - ECG (at least twice weekly) - to detect conduction disturbances, which may indicate
development of an aortic root abscess in aortic valve infection - Blood tests (twice weekly) - ESR, CRP, full blood count and U&Es
- Duration of antibiotics will depend on clinical response as well as local microbiology
guidance: patients may need 6 weeks or more of treatment
Indications for surgical management in IE?
- Moderate to severe cardiac failure due to valve compromise
- Valve dehiscence
- Uncontrolled infection despite appropriate anti-microbial therapy
- Relapse after optimal medical therapy
- Threatened or actual systolic embolism
- Coxiella burnetti and fungal infections
- Paravalvar infection (e.g. aortic root abscess)
- Sinus of valsalva aneurysm
- Valve obstruction
Signs that indicate instability in bradycardic patients?
Systolic BP < 90 mmHg, HR < 40 bpm, poor perfusion, and poor urine
output, ventricular arrhythmias requiring suppression or heart failure.
How can you assess axis deviation on ECG?
AVL most positive left axis deviation,
Lead 3 most positive then right axis deviation
How are bradycardias classified?
Absolute (<40bpm) vs relative
According to the pacemaker at fault: sinus node or AV node
What can sinus node dysfunction be?
Sinus bradycardia
Sick sinus syndrome (tachy-brady)
Sinus arrest alone or a spart of a vasovagal syncope
What might sinus node bradycardia be the result of?
Hypothyroidism Hypothermia Sleep apnoea (Less common) Rheumatic fever Viral myocarditis Haemochromatosis Pericarditis Amyloidosis
When is a pacemaker indicated in sinus node disease?
WHen pts are symptomatic
In sinus node bradycardia what is seen on ECG?
NSR (ie. every QRS is preceeded by a p wave) with slow rate
What is the PR interval in first degree AV block?
Over 0.2 seconds
When should higher degrees of AV block be looked for?
In patients presenting with syncope of diziness
Where can complete AV block occur?
Above the AV node at the His region (narrow complex escape and usually
well tolerated such as congenital complete heart block)
OR
Beneath the AV node with broad complex escape (not well tolerated).
Causes of third degree AV block?
Inferior STEMI (resloves in hours to days)
Anterior (infranodal) MI (more ominous)
Severe hyperkalemia
What drugs can be used to treat haemodynamically unstable complete heart block?
Atropine
Isoprenaline
What is required to inform longterm management of AF?
Baseline echocardiogram
How do DOACs work?
inhibit factor Xa (apixiban, rivaroxaban and edoxaban)
OR
directly inhibit thrombin (dabigatrin)
When should diltiazem/verapamil NOT be used in patients with AF who are having rate control?
LVEF < 40%
How can the Valsalva manoeuvre be performed?
having the patient bear down as though having a bowel movement or blowing hard into a syringe to move the plunger
How and when should carotid sinus massage be peformed?
Carotid massage is another vagal manoeuvre that can slow AV nodal conduction. Massage
the carotid sinus for several seconds on the non-dominant cerebral hemisphere side. This
manoeuvre is usually reserved for young patients. Due to the risk of stroke from emboli,
auscultate for bruits before attempting this manoeuvre. Do not perform carotid massage on
both sides simultaneously. Wait at least 10 seconds before trying the other side.
Rapid broad complex tachycardia shortly after STEMI is nearly always what?
VT
For how long should patients stay on anticoagulation following sucsessful DC cardioversion?
Following elective DC cardioversion for AF, anticoagulation should be continued even if sinus rhythm is maintained (lifelong)
What congenital defect is radio-femoral delay associated with?
Radio-femoral delay is associated with coarctation of the aorta
First line management of HTN in diabetic pts?
Hypertension in diabetics - ACE inhibitors/A2RBs are first-line regardless of age
ECG changes in a PE?
Sinus tachycardia
S1Q3T3 is demonstrated by a deep S-wave in lead I, a Q-wave in lead III and an inverted T-wave in lead III. It is associated with PE, however, it is neither sensitive nor specific for the condition and would not be the most common finding.
Why should verapamil never be taken with beta blockers?
Verapamil and beta-blockers should never be taken concurrently - possibility of heart block and fatal arrest
(the next line for prophylaxis of angina is Nicorandil if Dihydropyridine CCB not suitabe/contraindicatd)
Can use amplodpine as non-cardiselective (Dihydropyridine)
First line prophylaxis of angina?
Beta blocker
DO NOT MIX WITH Nondihydropyridine CCB
When should cardiac tamponarde be considered?
elevated JVP, persistent hypotension and tachycardia despite fluid resuscitation in a patient with chest wall trauma
Initial managment of cardiac tamponade?
Pericardial needle aspiration
What causes rheumatic fever?
Rheumatic fever develops following an immunological reaction to recent (2-6 weeks ago) Streptococcus pyogenes infection.
Pathogenisis of rheumatic fever?
Streptococcus pyogenes infection → activation of the innate immune system leading to antigen presentation to T cells
B and T cells produce IgG and IgM antibodies and CD4+ T cells are activated
there is then a cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry
the cell wall of Streptococcus pyogenes includes M protein, a virulence factor that is highly antigenic. It is thought that the antibodies against M protein cross-react with myosin and the smooth muscle of arteries
this response leads to the clinical features of rheumatic fever
Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever
Major criteria for Rheumatic fever?
erythema marginatum (ring lesions)
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 is the minor criteria for Rheumatic fever?
raised ESR or CRP
pyrexia
arthralgia (not if arthritis a major criteria)
prolonged PR interval
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
How does ventricular septal defect present?
Heart failure after a few weeks or asymptomatic, pansystolic murmur at lower left sternal edge and louder P2
What type of murmur is ToF?
ejection systolic murmur
How might a thiazide or thizaide like diuretic lead to hypokalemia?
Enhcanced Na+ delivery results in K+ loss in the collecting duct
When VF/pVT are shocked by a defib, when should adrenaline and amiodarone be administered?
If VF/pVT persists, only after a third shock should adrenaline 1 mg IV and amiodarone 300 mg IV be administered.
Importance of Isosorbide mononitrate post - MI?
Isosorbide mononitrate may be important in managing symptoms yet it has no proven mortality benefit following a myocardial infarction
When should NSTEMI be managed by PCI?
Pt unstable
Grace score indicates to
Dressler’s syndrome vs classic pericarditis?
Dressler’s syndrome is a seperate clinical phenomenon and is not generally seen in the first two weeks following a myocardial infarction (takes time for immunoglobulins to develop)
How might Left ventricular free wall rupture present?
Sudden onset dyspnoea Post anterior MI Hypotensive Elevated JVP Muffled heart sounds Widespread crackles on ascultation of chest Low O2 sats
CARDIAC TAMPONADE
What second line treatment is partcularly effective in pts of Afro-Carribian origin?
Hydralazine + nitrate
What is Takaysau’s arteritis?
Takayasu’s arteritis is a vasculitic disorder generally affecting young Asian women. It affects the aorta and its branches and causes both systemic features and those specific to which vessels coming off of the aorta are affected.
Medical management post ischemic stroke?
Aspirin 300 mg daily for 2 weeks should be given immediately after an ischaemic stroke is confirmed by brain imaging. Following this, clopidogrel 75 mg daily should be given long-term -if it can be tolerated and is not contraindicated.
What does malignant HTN usually involve?
Malignant hypertension usually involves severe hypertension and bilateral retinal hemorrhages and exudates
Poorly controlled hypertension, already taking a calcium channel blocker - add what?
Poorly controlled hypertension, already taking a calcium channel blocker - add an ACE inhibitor or an angiotensin receptor blocker or a thiazide-like diuretic
How should palpitations be investigated after initial bloods/ECG?
Palpitations should first be investigated with a Holter monitor after initial bloods/ECG
What is first line investigation for stable chest pain of suspected coronary artery disease aetiology
Contrast-enhanced CT coronary angiogram is the first line investigation for stable chest pain of suspected coronary artery disease aetiology
How can thiazides cause gout?
Thiazide diuretics reduce uric acid excretion from the kidneys
What kind of inheritance is hypertrophic obstructive cardiomyopathy?
Autosomal dominant
What is indapamide?
Thiazide diuretic
Management of HOCM?
An implantable cardioverter-defibrillator can be inserted to reduce the risk of sudden cardiac death in HOCM
Which part of the QRS complex is used for synchronisation in DC cardioversion?
R wave
What GI complication Nicorandil associated with?
Nicorandil is associated with ulcers that can occur anywhere along the gastrointestinal tract.
What antibiotic may interact with a statin to cause cardiomyopathy?
Clarithromycin
What electrolyte disturbance can lead to long QT syndrome?
Hypokalaemia can lead to long QT syndrome
Influence of diuretics in HF?
Improved symptoms
Does not improve mortality
What is dextrocardia associated with on ECG?
Dextrocardia is associated with an inverted P wave in lead I, right axis deviation, and loss of R wave progression
Mechanism of action of alteplase?
Activates plasminogen to form plasmin
Patients with bradycardia and signs of shock require what?
500micrograms of atropine (repeated up to max 3mg)
When is withholding warfarin for one day and monitoring INR appropriate
Withholding warfarin for one day and monitoring the INR is recommended in a non-bleeding patient with INR 5.0-7.9. This is inappropriate in a bleeding patient.
When should vitamin K be given to patients on Warfarin?
Stopping warfarin and giving oral vitamin K 3mg is recommended in a non-bleeding patient with INR >8.0. IV vitamin K should be given over oral vitamin K in a bleeding patient.
When should IV vitamin K and prothrombin complex be given to a patient with warfarin?
Stopping warfarin and giving IV vitamin K 5mg and prothrombin complex concentrate is recommended in a patient with a major limb or life-threatening bleed.
What is Coarctation of the aortic valve associated with?
Coarctation of the aorta can arise sporadically or can be associated with underlying medical conditions. Turner’s syndrome is the most well-known, but in a large number of cases (up to 60%), patients have a concurrent bicuspid aortic valve. This can in itself cause an ejection systolic murmur and can give an increased risk of the valve becoming stenosed.
What Grace score warrents PCI?
A risk higher than 3% (as is the case with this patient) indicates that the patient should undergo PCI within 72 hours of hospital admission
What causes VF?
VF is caused by chaotic and uncoordinated electrical activity in the ventricles and as such produces an irregular rhythm with broad QRS complexes of differing amplitudes.
HOCM may cause a murmur similar to aortic stenosis, what can give a major clue to differentiate between the two?
HOCM is classically a disease of the young. It does cause an ejection systolic murmur similar in quality to aortic stenosis, but it would be rare for a patient with significant HOCM to survive to middle-older age without diagnosis and intervention.
Causes of ejection systolic murmur?
Aortic stenosis
Pulmonary stenosis
HOCM
Typical use of flecainide?
Flecainide is classically used to cardiovert patients who have acutely gone into atrial fibrillation. It has an emerging role in the management of SVT; however would still not be used before attempting vagal manoeuvres. It is contraindicated if there is known structural heart disease.
Vasovagal syncope vs seizure?
Vasovagal syncope is commonly positional, such as here following a long period of standing on the tube, and is often described as being preceded by tunnel vision or vision “closing in”. A short period of convulsions can be normal. It can be differentiated from proper seizure activity by the lack of a post-ictal phase (rapid return in GCS)
Cardiogenic shock
increased SVR (vasoconstriction in response to low BP)
increased HR (sympathetic response)
decreased cardiac output
decreased blood pressure
Hypovolaemic shock
blood volume depletion
e.g. haemorrhage, vomiting, diarrhoea, dehydration, third-space losses during major operations
increased SVR
increased HR
decreased cardiac output
decreased blood pressure
Septic shock
occurs when the peripheral vascular dilatation causes a fall in SVR
similar response may occur in anaphylactic shock, neurogenic shock
reduced SVR
increased HR
normal/increased cardiac output
decreased blood pressure
Orthostatic hypotension (A fall in SBP of >20mmHg on standing) accompanied by an exaggerated increase in HR is indicative of orthostatic hypotension due to what?
Hypovolemia
Anaemia
Postural orthostatic tachycardia syndrome (POTS) is characterised by what heart rate changed?
Postural orthostatic tachycardia syndrome (POTS) is characterised by an exaggerated heart rate increase of >30bpm or to >120bpm.
ALS - non shockable rhythm?
give 1 mg adrenaline ASAP if non-shockable
Long PR interval?
Heart block
Short PR inteval?
Acessory pathway
What might causes a broad QRS?
BBB, Hyperkalemia
What electrolyte disturbances can prolong QT?
Hypocalcemia
Hypokalemia
In STEMI where will recipricol changes be on ECG?
Posterior – anterior reciprocal changes
Anterior – inferior reciprocal changes
Inferior – lateral reciprocal changes
Lateral inferior or septal reciprocal changes
Septal – posterior reciprocal changes
What HTN agent is not used in post MI patients?
CCB
MI complications?
Cardiogenic shock VT and arrest Mitral regurg (1 week) VSD Free wall rupture Ventricular aneurysm Dresslers syndrome CHronic hf
Max dosage of GTN spray?
2 every 5 mins
up to 6 sprays
What might be seen in stable angina resting ECG?
Axis deviation
OLD BBB
Tall QRS
Poor R wave progression
Chronic management of MI?
Most common cause of RHF?
LHF
Lung disease - cor pulmonale
What sided HF peripheral odema?
Right sided
What side HF pulmonary odema?
Left sided
Acute HF management?
Sit up
O2
IV furisomide bolus
?CPAP
Management of chronic HF?
Furisomide - symptoms only
Beta blocker + ACEi
2nd line
Sprinolactone (if potassium less than 4.5)
3rd line Nitrates
Digoxin
What might a specialist start when triple antiHTN therapy has failed in GP (ie. fourth line management)?
Sprinolactone if K+ less than 4.5
Otherwise Atenolol
Malliginant HTN?
Stage 3, over 180/110
Pre HTN?
120/80-140/80
Stage 2 HTN
160-180
Management of malignant HTN?
Symptomatic >180/110
Asymptomatic >220/120
Immediate refferal
Management of malignant HTN?
Symptomatic >180/110
Asymptomatic >220/120
Immediate refferal
Management of HTN in pregnancy?
Labetalol
Adenosine is used in paroxysmal SVT when vagal manouvers are failed, how many times would you push it before 3rd line management, and what is the 3rd line management?
x3 fast boluses
3rd - IV verapamil
Broad complex tachycardias?
VT - quite common cause of syncope in elderly pts with bgx of ischemic heart disease
Torsardes de pointes
Ventriclar fibu
VT vs Torsardes?
Similar morphology
TORSARDES has varying amplitudes
Shockable rhythms?
Pulseless VT
Pulseless VF
Why should IV amiodarone be used and NOT adenosine in WPW?
Adenosine is AV blocking
Which type of bundle branch block is always pathological
Left
right can be normal in young, tall and thin
LBBB
Broad QRS
Negative V1
Managed by cardiac pacing and pacemaker if symptomatic
What might a new RBBB suggest?
PE
What does an old RBBB suggest?
RVH
RBBB
Broad QRS,
+tive V1
Pacing and pacemaker if symptomatic
Bifasicular block can be identified by what?
RBBB and LAD
What does syncope suggest in aortic stenosis?
Severe AS
Most important initial management of SEVERE aortic stenosis?
Stop ACEi
As it reduces peripheral vascular resistance, may become suddenly hypotensive as blood not being pumped past stenosis - shock
What inherited syndrome can cause aortic stenosis?
Turners (bicuspid valve)
Mitral regug commonly causes complications post MI, such as what?
Pulmonary HTN
AF
Where is mitral stenosis more common and why?
Developing countries
Rheumatic/scarlet fever heavily associated with
PTS HAVE MALAR FLUSH
Why does mitral stenosis cause a malar rash?
CO2 retention due to pulmonary stasis in the lung
Pericarditis vs myocarditis
Most are typically post viral
Pericarditis CAN be post MI
Myocarditis mimics ACS
Pericarditis mimics pleuretic chest pain
Raised JVP or signs of HF more common in myocarditis
Global concave ST elevation, no reciprical changes in pericardits + PR depression
ECG usually normal in myocarditis
Troponin will be high in myocarditis but not in pericarditis
Myocarditis requires echo and BNP
How are myocarditis and pericarditis managed?
NSAIDs and colchicine
In myocarditis, if HF, also include:
ACEi +/- Betablocker
q89w
Examples of CCB that are safe alongside beta blockers?
Amlodipine
Felodipine
What level of total cholestroal warrents further investigation for familial primary hyperlipidaemia?
7.5+
Causes of macrocytic anaemia?
Alcohol B12 def Cirrhosis/comp reticulocytosis Drugs (cytotoxic agents, phenytoin)/Dysplasia (myelodysplastic syndrome) Endocrine (hypothyroid) Folate def/ fetous - preg
Hypertrophic obstructive cardiomyopathy findings on echo?
Asymmetric septal hypertrophy and systolic anterior movement (SAM) of the anterior leaflet of mitral valve on echocardiogram or cMR support HOCM
High levels of BNP can have causes other than heart failure, such as what?
age over 70 years, left ventricular hypertrophy, ischaemia, tachycardia, right ventricular overload, hypoxaemia (ie pulmonary embolism), renal dysfunction (eGFR less than 60 ml/minute/1.73 m2), sepsis, chronic obstructive pulmonary disease, diabetes, cirrhosis of the liver
Target INR for anti coag?
2-3 most pts
2.5-3.5 if mechanical valve
What happens in aortic dissection?
Bleeding into the vessel wall, most commonly affects the ascending aorta and aortic arch but can affect any part of the aorta
Blood enters between intima and medial layers of the aorta
False lumen full of blood formed in the aorta
In STEMI how should a patient be managed whilst waiting for A PPCI?
Reassure Oxygen Morphine Aspirin 300mg Nitrates (sublinguial GTN) Clopidogrel 300mg (older, stable) or ticagrelor usually Emetics(anti) IV metoclopramide
Signs consistent with constriction pericarditis?
Increase JVP on inspiration - Kussmauls sign
Third heart sound (RSHF)
Peripheral odema (RSHF)
Calcified pericaral sac
Causes of low QRS voltage on ECG?
Pericardial effusion (MASSIVE) Obesity Emphysema Myoxedema Pneumothorax Pleural effusion Infiltrative myocardial diseases — i.e. restrictive cardiomyopathy due to amyloidosis, sarcoidosis, haemochromatosis Constrictive pericarditis Scleroderma
SVT defnition
Signal from atria over 100 BPM
What ECG changes may be seen on PE?
- Sinus tachycardia
- Right bundle branch block (broad QRS, large R wave in V1 and V2, broad deep S wave in V5, V6)
- Right ventricular strain pattern (ST depression and T wave inversion in right precordial leads V1-3 +/- V4, inferior leads II, III, aVF, often most pronounced in lead III as this is the most rightward facing lead)
- Right axis deviation (QRS is POSITIVE (dominant R wave) in Lead II, Lead III and aVF, QRS is NEGATIVE (dominant S wave) in Lead I)
- Right atrial enlargment ( pronounced notch in the P wave)
S1 Q3 T3
- S wave present lead 1
- Q wave present lead 3
- T wave invesion lead 3
COPD vs Right sided heart failure
PND - HF Sputum - pink in HF, white in COPD Palipitations - HF Breathlesness - either Tightness in chest - COPD
Why is erythromycin best avoided in pts with long QT syndrome?
May further prolong QT interval
Can cause arrythmia
Which organisms in IE has the highest mortality?
Staph aurues
TTE is prefered when?
When ventricular surfaces of valves are being investigated
TOE is preffered when?
Aortic/atrial valve surface
MV or perivalvular complications
What is reccomended f patients treated with PCI for MI are experiencing pain or haemodynamic instability post PCI?
CABG
ECG in LVH?
The ECG shows large R waves in the left-sided leads (V5, V6) and deep S-waves in the right-sided leads (V1, V2). There is also ST elevation in leads V2-3.
New widening QRS complexes and an RSR’ pattern in V1
RBB
ECG shows new widening QRS complexes and a notched morphology of the QRS complexes in the lateral leads
LBB
Frank Starling Law
Stroke volume increasing as the left ventricular end diastolic volume increases
Increased stretch on cardiocytes causes a more forceful contraction
In HrEF increased end diastolic volume leads to decreased stroke column as the pharmacological limit is passed
What antibiotics should be added in endocarditis of a prosthetic valves
SA add rifampicin and gentamicin
Tall tented T waves + flattened P waves
Hyperkalemia
ECG changes (in order of severity) are:
Tall tented T-waves
Flattened P-waves
Prolonged PR interval
Widened QRS complexes
Idioventricular rhythms
Sine wave patterns
VF/asystole
PR interval prolongation in a patient with Infective Endocarditis is an indication for what and why?
PR interval prolongation in a patient with Infective Endocarditis is an indication for surgery as it can be secondary to aortic root abscess
