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
