CARDIOVASCULAR Flashcards
Define atherosclerosis
Inflammatory process characterised by Accumulation of lipids, macrophages, and smooth muscle cells in the intima of large and medium sized arteries, encased within a fibrous cap.
name 4 main constituents of an atheromatous plaque
An atherosclerotic plaque is a complex lesion consisting of :
Lipid
Necrotic core
Connective tissue
Fibrous “cap”
Eventually the plaque will either occlude the vessel lumen resulting in a restriction of blood flow (angina), or it may “rupture” (thrombus formation – death).
Taken form netter illustrated pathology
What is the primary cause of atherosclerosis?
Endothelial cell damage.
Outline the progression of atherosclerosis.
- High levels of cholesterol damages endothelium.
- LDLs pass in and out of the arterial wall in excess and accumulate in it, and there is undergoes oxidation and multiplies, leading to inflammation
- The inflammation releases chemoattractants, which attracts Macrophages try to break down, LDLs, turning into foam cells, which produce a LIPID CORE/FATTY STREAK
- This inflammatory reaction leads to tissue repair, so the smooth muscle proliferates forming a fibrous cap that encloses the lipid core.
Taken form netter illustrated pathology
Fully formed atherosclerotic plaques, can rupture -why is this?
What would a rupture plaque lead to?
The caps can rupture, this is down to the enzymatic activity breaking down the plaque more than it is being laid down. ==> this imbalance can be triggered by pneumonias/infection.
===>The microvessels in the plaque will Haemorrhage, which will lead to thrombus (clot formation and a subsequent blockage of the vessels
taken from Prof Simon Cross lecture
Name some measures to prevent atherosclorosis.
- Smoking cessation
- Control of blood pressure
- Weigh reduction
- Low dose aspirin - inhibits the aggregation of platelets, advised for people
with clinical evidence of atheromatous disease - Statins - cholesterol reducing drug
What are some risk factors for atherosclerosis?
What is the most significant risk factor for atherosclerosis?
age, gender, genetics, smoking, high blood pressure, high cholesterol, diabetes, and obesity.
Hypercholesterolemia is most significant RF for atherosclerosis
development
Atherosclerosis - when the endothelium is damaged, what happens that leads to inflammation?
the accumulation of LDL-cholesterol in the artery wall, which leads to the activation of inflammatory cells
Atherosclerosis - Once the endothelium wall is inflamed, what will begin to accumulate? What does this lead to?
As the endothelial cells become damaged, they begin to accumulate fats, such as cholesterol, triglycerides, and phospholipids. These fats oxidize and cause the formation of fatty plaques in the artery wall.
What medications can help treat Atherosclerosis?
statins - Lower Cholesterol
blood pressure-lowering medications
Aspirin
Anticoagulants
How does Aspirin help reduce cardiovascular disease? What type of drug is it?
It is a NSAID, can be over the counter, in cardiology, can act As an antiplatelet
It IRREVERNSIBILY blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation.
taken from IHD Symposium - Acute coronary syndromes - Prof Robert Storey
What type of Drugs are
a) Clopidogrel and
b) GPIIba antagonists? What is their effect on the CV system?
a) P2Y12 receptor blockers - Drugs like Clopidogrel block the P2Y12 receptor to Reduce platelet activation
b) These block glycoprotein IIb/IIIa receptors on their platelet’s plasma membrane and inhibiting fibrinogen binding - also reduce platelet activation.
*BOTH ANTIPLATELET
taken from IHD Symposium - Acute coronary syndromes - Prof Robert Storey
How does Heparin work?
Heparin binds to antithrombin III, an enzyme inhibitor, makes it more reactive and flexible
Once AT is activated, it is able to prevent the action of thrombin, factor Xa, and other proteins.
LMWH - Dalteparin
How does Warfarin work?
Warfarin blocks the enzyme VKORC1, which is crucial for activating vitamin K. ==> decreases in amount of vitamin K available, which ultimately weakens the body’s ability to form clots.
The vitamin K dependant clotting factors are 10, 7, 2 9.
Warfarin will affected the Prothrombin time, -(looks at common and extrinsic pathway) making it increased.
What do anticoagulants do? What do they inhibit? Give some examples
Anticoagulants work by preventing the formation of blood clots. They do this by Inhibiting thrombin (factor 2 in CC) in the body that are involved in the clotting process
Eg Warfarin, DOACs like Apixaban
DOACs inhibit factor 2 and 10a (think - all have Xa in their name)
Outline what Acute Coronary Syndrome is. What 3 conditions are associated with it?
It’s complex set of symptoms caused by reduced blood flow to the heart. It is typically caused by a blockage in the coronary arteries
Covers a spectrum of diseases from **Unstable angina, NSTEMI, to a Myocardial Infarction with ST wave elevation, STEMI.
What is the most common cause of death in the UK?
Coronary heart disease
What is the incidence of CHD? (new cases per year) what % of hospital admissions does it account for each year?
300,000
3%
How many deaths occur with in 2 hours of the onset of Symptoms in MI?
What percentage of MI cases are fatal?
50% of deaths occur within 2 hours of onset of symptoms
15% of cases of MI are fatal
What is the main cause of unstable angina, NSTEMI, and STEMI?
What are some other causes of these?
Unstable Angina and NSTEMI - Partial occlusion of coronary arteries
STEMI - complete or almost complete blockage of the coronary arteries
Most common cause -
Rupture of a fibrous cap of coronary artery plaque
Other causes:
- Coronary Spasm leading to less blood supply to myocardium
- Coronary Embolism
- Chest trauma
- Recreational drug use like Cocaine
What is the pathophysiology behind the main cause of ACS?
Rupture of a fibrous cap of coronary artery plaque
Leads to the Release of the lipid-rich atherogenic core,
Leads to causes adhesion, activation, and aggregation of platelets.
This initiates the coagulation cascade, causing a superimposed thrombus forming, leading to myocardial ischaemia/infarction
What are the risk factors for ACS?
Non-modifiable
* Age
* Gender (male)
* FH of IHD – only significant if symptoms presented before the age of 55 in the relative
Modifiable
* Smoking
* Hypertension
* Diabetes
* Hyperlipidaemia
* Obesity
* Sedentary lifestyle
Taken from almostadoctor
What are the Key clinical presentations for unstable angina
○ Cardiac chest pain AT REST
○ May have crescendo pattern (it gets worse and worse more readily)
New onset angina
50% of patients with unstable angina will get an infarction within 30 days if left untreated
What are some key symptoms of MIs?
Acute chest pain >15 minutes
Pain that radiates to both arms, or just right arm, arms or jaw
Pain can also radiate down epigastrium (upper central part of abdoemen, or back
Diaphoresis - Sweating
Vomiting
Exertional chest pain
Breathlessness - Can be the only symptom
Syncope - Fainting
Distress, feeling of impending down
Patients with MIs can present with no pain!!
What is a Silent MI? What % of patients present with it, and it what populations is it most common?
MI without chest pain
30% of case of MI present without chest pain.
This is particularly important in:
* Women
* Those with diabetes
* The elderly
What are key symptoms that could be due to a silent MI? What Significant historical features might you see in someone with a silent MI?
Other symptoms associated with a silent MI include:
Syncope
Pulmonary oedema
Epigastric pain
Vomiting
Acute confusional state
Stroke
Diabetic hyperglycaemia
Significant historical features include:
Shortness of breath – especially if on exertion (“SOBOE”)
Generalised weakness
Dizziness
CHECK IF PATIENT HAS HAD CHEST PAIN IN THE LAST 12 HOURS, IF THEY ARE NOT HAVING CHEST PAIN NOW
What are some signs of MIs?
Pallor - due to sympathetic activity
Sweating
Tachycardia
High or low blood pressure
Heart Murmurs eg systolic murmur in Mitral regurg
S4 heart sound - due to impaired left ventricle diastole
Signs of Pulmonary Oedema
Palpitations
Raised Troponin
ECG abnormalities
What investigations would you order for ACS/Suspected MI?
What would you look for on examination
ECG, as soon as possible
Blood Troponin Levels
FBC, Blood glucose,
Count Platelets -(due to Thrombocytopaenia, (low blood platelets) potentially occurring
Chest x-ray to look at other causes of central chest pain
Do a cardiac examination for
Pulse
BP
JVP
Murmurs
How would you rule out MI in suspected ACS patients?
Measure High sensitivity cardiac troponin with 1 hour.
there will be no dynamic rise above the 99th percentile in patients with unstable angina
What are the ranges of troponin that are normal, and that could be indicative of an MI?
Troponin values <14ng/l normal = no MI, 14-30 ng/l = possible MI, >30ng/l = definite MI
ACS ECGs - what would you seen on an ECG with someone with unstable angina?
What is the gold standard test for diagnosing unstable angina, if Troponin test is -ve
An absence of ST elevation
typically no ECG changes
ST depression (indicates a worse prognosis), transient ST elevation, and T-wave changes may be seen
May also be Normal!!!
can be similar to NSTEMI
Gold standard test used to diagnose this condition - Angiography
ACS ECGs - what would you see on an ECG with someone with NSTEMI? How would you distinguish between unstable angina and NSTEMI?
An absence of ST elevation
T-wave inversion
Hyper-acute T waves
ST depression
May also be Normal!!!
Same as unstable angina
Distinguish with High Sensitivity cardiac troponin testing. Will be elevated in NSTEMI
picture source unknown
Outline how you carry out a High sensitivity troponin test. What would you see in MIs that you wouldn’t see in other conditions that can cause raised troponin?
Measure Troponin twice, 2 hours apart, with in 3 HOURS of onset of chest pain
A single negative troponin test is acceptable as a ‘rule out’ (for ACS) if it is >3 hours since the onset of pain - aka Unstable angina
A positive test is defined as an increase in troponin between the two tests.
- On average, and 20% rise is accepted for a diagnosis of NSTEMI
In MIs , you expect Troponin levels to rise
In other conditions that can raise troponin, the troponin levels won’t change much as the issue is ongoing
Peoples troponin levels vary, so look at change in level other level itself
What are other causes of Raised troponin other than MIs?
Causes include:
Renal failure
Myocarditis
PE
Pericarditis
Heart failure
Arrhythmia
What ECG changes would you see in a STEMI, immediately??
Peaked T wave (very tall T wave)
Raised ST-segment - this can return to normal within a few hours
Signs of a New LBBB —> M shaped waves in V6 - LBBB - become and change shape (wiLLiaM)
For any patient with new onset chest pain and LBBB on ECG you need to compare to an old ECG to see if the LBBB is new. If none is available, consider STEMI until proven otherwise.
taken from osmosis
What ECG changes would you see in a STEMI,
a) within 24 hours
b) within days
a) Inverted T waves – this may or may not persist
ST segment returns to normal.
Raised ST segments may persist if a left ventricular aneurysm develops
b) Pathological Q waves form – these may resolve in 10% of cases
Q wave is pathological if it is >25% of the height of the R wave, and/or it is greater than 1small square in width, and/or greater than 2 square squares in height
Q waves are also a sign of a previous MI – the changes in Q waves are generally permanent
picture credit - unknown
What are some differential diagnosis for ACS?
Cardiac
* Angina
* Pericarditis
* Myocarditis
* Aortic dissection
Pulmonary
* PE
* Pneumothorax
* Anything that causes pleuritic chest pain
Oesophageal
* Oesophageal reflux
* Oesophageal spasm
* Tumour
* Oesophagitis
Any of the other 2 conditions in ACS
Taken from almostadoctor
What is the first line acute management of ACS?
MONA
Morphine - For pain relief
Oxygen - ONLY IF SATS ARE LESS THAN 94% -
don’t need to give it if not!
Nitrates (GTN SPRAY) - typically fondaparinux in Sheffield - A GTN, Glyceryl Trinitrate
Aspirin 300mg chewed to increase absorption
Urgent ECG, IV access, Take history
What are nitrates, like GTN? Why are they given in ACS, and when would you not give them?
Nitrates like GTNs decrease amount of oxygen being used by heart.
==> Helps to reduce the workload on heart, prevents further damage to heart muscle.
Also help to open up the blood vessels, increasing blood flow to the heart
BUT don’t give with systolic BP <90, or with a HR <50, or left ventricular heart failure
As they lower blood pressure -
Once diagnosis of STEMI is confirmed, what is the definitive management?
Refer to cardiology urgently
First line, definitive
Percutaneous Coronary Intervention - only suitable if done within 2 HOURS OF ONSET
If PCI/angioplasty is not Available/over 2 hours - give Fibrinolysis with IV Tenecteplase
-
Aspirin, AND a PY12 inhibitor, eg
clopidogrel/ticagrelor
Give Heparin (anticoagulant)
Give Glycoprotien IIb inhibitor
Do not give anticoagulant therapy if the patient is likely to be eligible for primary PCI.
BUT – DONT GIVE FIBRINOLYSIS/THROMBOLYSIS TO THOSE WITHOUT ST ELEVATION
How long is a patient with a STEMI eligible for a PCI?
Only offer a PCI if the patient is presenting within 12 hours on symptoms onset, and the PCI can be delivered within 120 mins
Can consider it if presneting more tahn 12 hours after symptoms if still continuing with myocardial ischaemmia or cardiogenic shock
What do you do with your patient with suspected ACS/NSTEMI, who is unstable?
What is not considered in NSTEMI?
You need to get urgent input from seniors to arrange immediate invasive coronary angiography (with the intent to perform revascularisation) for any patient who has suspected NSTEMI and is clinically unstable
- it looks at the vessels of the heart with a dye
Do not wait for the results of troponin testing.
Thrombolysis is NOT INDICATED for NSTEMI
What things would lead to a suspected NSTEMI patient being deemed unstable while you wait for troponin test to come back, that would mean that arrange an angioplasty?
Suspected NSTEMI and Clinically unstable - This includes any patient with:
Ongoing or recurrent pain despite treatment
Haemodynamic instability (low blood pressure or shock); see our topic Shock
Dynamic ECG changes
Left ventricular failure
A life-threatening arrhythmia (ventricular tachycardia or ventricular fibrillation)
Outline what a Primary PCI is
The urgent use of PCI (Percutaneous Coronary intervention) known as angioplasty blood vessel open.
A balloon tipped catheter is entered into the body, normally in femoral or radial artery
A guiding catheter is passed up the coronary artery, so radiopaque iodine based dye can be passed through the coronary arteries so they can be viewed on x-ray
A balloon tipped catheter is placed and inflated in the right place and usually a stent in placed in the artery and is expanded by the pressure of the inflating balloon
Normal physiology - what does the enzyme PCSK9 do?
PCSK9 attaches itself to the LDL receptor (LDLR) found on liver and other cellular membranes and causes it to break down, preventing it from receiving LDL particles from outside of the cell and reducing the amount of LDL particles in circulation.
What are PCSK9 inhibitors? What are they used for?
They are monoclonal antibodies that inhibit PCSK9 protein in the liver which leads to improved clearance of cholesterol from the blood. Therefore used to treat Hypercholesterolaemia
What is thrombolysis? When would you use it in ACS?
The second line treatment for STEMI
Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous.
From zerotofinals
How can you assess whether an NSTEMI patient would qualify for a PCI?
A Key part of management!!!
GRACE SCORE
This scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI:
<5% Low Risk
5-10% Medium Risk
>10% High Risk
If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.
Taken from zerotofinals
What is the definitive management for unstable angina?
- If the history is convincing, but the investigations are normal, consider unstable angina
- Consider a risk score – such as the HEART score to help you decide whether or not to discharge home, or refer to cardiology for admission
Patients should undergo ECG stress testing (‘treadmill test’)
What is the long term management for all ACS patients?
Clopidogrel or equivalent - STOP PLATELET ACTIVAATION
Beta Blocker or ACE inhibitor or Angiotensin II receptor antagonist
Statins
Monitor Blood Glucose in Diabetic Patients
Name some secondary prevention measures (non medicinal) for ACS.
Exercise,
Smoking cessation
Reduction in weight
Reduction in alcohol intake
Dietary modifications - eg High in oily fish, fibre, fresh fruit and veg, Low in Saturated fat
Also don’t fly for 2 months, no sex for a month
What are some medications used in secondary prevention for ACS?
COBRA-A
C – Clopidogrel – antiplatelets
O – Omacar – Omega 3
B – Bisoprolol – β-blocker
R – Ramipril – ACE-i
A – Aspirin
A – Atorvastatin – very potent statin!
What are some complications of an MI?
DREAD:
Death,
Rupture of septum or papillary muscles (which could lead to ischaemic MR),
oEdema (Heart failure),
Arrhythmia and Aneurysm, Dressler’s syndrome.
What is the early mortality of MIs in
a) Outside hospital
b) inside hospital
30% out of hospital
15% in hospital
What is the late mortality of MIs in
a) First year
b) annually thereafter
5%
2-5%
What pharmacological medicines would you give to treat ACS in heart failure patients
Diuretics, ACEI, beta blocker, aldosterone antagonist
(spironolactone, epleronone
What are the main anti anginal therapies?
beta blocker, nitrates, calcium antagonist
Cardiac tumours are rare - but what is the most common primary cardiac tumour? Where is it most commonly found
Cardiac Myxoma - have a bias towards the atria. Often harmless, but can be very bad if they block the mitral valve.
What % of the population suffer from Hypertension?
25%
Simply put, what is pericarditis? What is the triad that clinically characterises it?
Inflammation of the Pericardium
It is characterised clinically by a triad of chest pain, pericardial friction rub, and serial ECG changes.
Normal Physiology - what are the layers of the pericardium?
- Fibrous Pericardium - This is the outermost layer and is composed of dense connective tissue.
- Parietal Pericardium - This is the middle layer and is composed of serous membrane.
- Visceral Pericardium/Epidcardium - This is the innermost layer and is composed of serous membrane. It is also known as the epicardium.
The fluid is located between the Parietal and Visceral Pericardium layers.
Normal Physiology - what is the functions of the pericardium?
- Fixes the heart in the mediastinum and limits its motion
- Prevents overfilling of heart, inextensible fibrous layer prevents the heart from increasing in size too rapidly
- Lubrication from the thin film of fluid between the two layers of serous pericardium reduces friction generated by the heart as it moves
Protection from infection – the fibrous pericardium serves as a physical barrier between the muscular body of the heart and adjacent organs prone to infection e.g. the lungs
In which group is pericarditis most common
When is is most likely to happen?
Acute pericarditis is more common in adults (typically between 20 to 50 years old) and in men.
In the UK, pericarditis is most commonly secondary to viral infection or MI
What are the common causes of Pericarditis?
Viral Infection
Acute MI
Dressler’s Syndrome
Autoimmune Conditions - Rheumatoid arthirits, SLE
Trauma/Surgery
Bacterial infections -
Malignancy
Metabolic disorders (uraemia)
What are the most common bacterial causes of pericarditis in:
People from developing countries
People with Prosthetic valves
People with normal valves in the developed world
Streptococcus viridans is the commonest cause in patients from developing countries with an absence of other specific risk factors.
alpha haemolytic
Staph. epidermidis is a more likely causative organism of infective endocarditis if the patient has prosthetic valves -coagulase negative
Staph. aureus is now the commonest cause in the developed world and is particularly likely if the patient is an intravenous drug user as is the case in this scenario. - coagulase positive
What viruses are most commonly associated with causing pericarditis?
What infection of pericardium do you often see in HIV patients?
coxsackie B virus, influenza, adenovirus and echovirus
- HIV – these patient may get staphylococcal pericarditis – which is often fatal
What are the 2 types of pericarditis you can get following an MI?
Post MI Pericarditis - occurs in about 20% of MI patients, most commonly with anterior MI and MIs with Massive ST elevation - (But reduced in Thrombolysis)
Dressler’s Syndrome - Pericarditis secondary to myocardial/pericardial damage, an autoimmune reaction by the body to damage Myocardium from a MI
(Antimyocardial antibodies are often found. Can occur anytime from few weeks to 2 years from an MI)
What are risk factors for pericarditis?
male sex
age 20 to 50 years
transmural myocardial infarction A heart attack that affects the entire thickness of heart wall
cardiac surgery
neoplasm
viral and bacterial infections
systemic autoimmune disorders
What are some main symptoms of Pericarditis?
- Central chest pain
○ Severe
○ Worsened on deepened breathing
○ Sharp and pleuritic (without constricting crushing character of ischaemic pain)
○ Releived by leaning forwards and sitting up - Dyspnoea
- Hiccups – phrenic involvement
- Fever
What are some investigations for suspected Pericarditis? What should you remember to do when investigating suspected pericarditis?
Bear in mind there is no specific diagnostic test.
Diagnoses should be based on clinical history – e.g. recent viral infection (+/- absence of risk factors for cardiovascular disease) -
Listen to chest - look for Pericardial friction Rub
ECG
FBC – there may be leukocytosis or lymphocytosis due to viral or bacterial infection
Echocardiogram - best
CXR
What is pericardial friction rub? Where is it best heard?
High pitched superficial scratching or crunching sound produced by movement of the pericardium.
It is diagnostic for pericarditis.
Usually heard in systole but may also be heard in diastole.
* It is classically heard in three, or two (‘to and fro’ rub) phases – i.e. this means it is heard 3 times or twice during one cardiac cycle
- The rubs are typically heard best with the diaphragm at the left lower sternal edge at full expiration
What would you see on an ECG of someone with Pericarditis?
Saddled ST elevation - distributed in both inferior and anterior leads – thus this helps to distinguish it from MI
PR depression
If both of these are present it is diagnostic of pericarditis
What is the management of Pericarditis?
Treat the underlying cause!
Colchicine - inhibits migrations of neutrophils to site of inflammation to reduce risk of occurrence
* 500mcg BD for 3 months
- PLUS
*Oral NSAID’s - Ibuprofen or Aspirin
- Do not use NSAID’s in the first few days after MI – as they associated with increased risk of myocardial rupture
What are some complications of Pericarditis?
- Pericardial effusion – Accumulation of fluid in the pericardial sac
- Cardiac tamponade – When there is enough pericardial effusion in the pericardium that it restricts diastolic ventricular filling (ability for heart to expand) and causes reduced BP and CO
- Chronic constrictive pericarditis – persistent inflammation of acute pericarditis causes the heart to be encased with a rigid fibrotic pericardial sac which prevents adequate diastolic filling of the ventricles
Normal Physiology - where is the pericardial cavity? What is found there?
What happens in a pericardial effusion?
In-between the two layers of serous pericardium, (Parietal and Visceral) where there is lubricating fluid - here there is potential space
Pericardial effusion is when the potential space of the pericardial cavity fills with fluid. This creates an inward pressure on the heart, making it more difficult to expand during diastole
Pericardial effusions/tamponade: What are the two main sources from which too much fluid comes from?
Increased venous pressure - so drainage from pericardial cavity is reduced -seen in Congestive heart failure/Pulmonary hypertension
Exudative effusions - seen in inflammatory processes, such as in the causes of pericarditis
What are some symptoms of
a) quick developing pericardial effusions
b) Slow developing pericardial effusions
a) Cardiac Tamponade
b) THINK - FULLNESS IN CHEST, COMPRESSING LOCAL STRUCTURES
aka
Chest pain
Shortness of breath
A feeling of fullness in the chest
Orthopnoea (shortness of breath on lying flat)
Phrenic nerve compression - Hiccups
Recurrent laryngeal nerve compression - hoarse voice
Osesphagus compression - Dysphagia
What would you see on examination of suspected Pericardial effusion/cardiac tamponade?
Quiet heart sounds
Pulsus paradoxus (an abnormally large fall in blood pressure during inspiration, notably when palpating the pulse)
Hypotension
Raised JVP
Fever (with pericarditis)
Pericardial rub (with pericarditis)
What investigations would you order for suspected pericardial effusion?
CXR – large heart
ECG – low voltage QRS complexes and sinus tachycardia
Echocardiogram
What are the management options for pericardial effusions?
Treatment of the underlying cause (e.g., infection)
Drainage of the effusion (where required)
eg Needle pericardiocentesis (echocardiogram guided),
Surgical drainage
Treat the pericarditis if necessary
Management:
Most pericardial effusions resolve spontaneously
If effusion recurs, excision of pericardial segment allows fluid to be absorbed through plural and mediastinal lymphatics
What is a cardiac tamponade?
Cardiac Tamponade is a condition where the heart become compressed by excess fluid in the pericardium. Compression causes reduced diastolic filling of the heart, which can cause cardiac arrest.
taken from almost a doctor
What are the causes of cardiac tamponade?
Traumatic injury – particularly penetrating injury – can lead to accumulation of blood in the pericardial sac. In trauma emergency setting it is life threatening
Pericarditis, pericardial effusion
Cancer
Iatrogenic - occur after cardiothoracic surgery
What is Beck’s Triad? When would you see it?
Becks Triad – occurs in about 1/3 of patients with cardiac tamponade
Hypotension
Distended Neck Veins
Muffled Heart Sounds
Taken from almostadoctor
What are some symptoms of a cardiac tamponade?
Dyspnoea
Elevated Jugular Venous pressure
Distant heart sounds
Tachycardia
Hypotension
Reduced exercise tolerance
Pulsus Paradoxus -Pulse fades/systolic BP decreases >10mmHg on inspiration
What is the management for a cardiac tamponade in
a) haemodynamically stable/pre tamponade
b) haemodynamically unstable/severe tamponade
c) if Pericardial effusion repeatedly reoccurs
a) anti-inflammatory treatment plus gastroprotection plus observation
b) emergency pericardiocentesis
c) effusion recurs, excision of pericardial segment allows fluid to be absorbed through plural and mediastinal lymphatics
What is pericardiocentesis/how is it performed?
Where a needed is inserted into the pericardium and fluid is drawn out.
The most common approach for pericardiocentesis is between the xiphoid and the left costal margin.
Initially, the needle is inserted at a 15-degree angle to pass under the costal margin. The needle is then lowered to a plane parallel with the chest and slowly advanced towards the tip of the left scapular, while aspirating
taken from bmjbestpractise
What is infective endocarditis?
What can it increase the risk of?
Infection of the heart valves and/or other endocardial structures within the heart e.g. septal defects, pacemaker leads, surgical patches etc.
Can increase the risk of embolism!!
Who used to be the most commonly affected group with Infective Endocarditis?
Nowadays, what groups of people are most likely to get IE?
In the past was most commonly seen in children with Rheumatic heart disease - Autoimmune condition, where body attacks heart
Nowadays, seen in
○ The elderly (in an ageing population)
○ IV drug abusers (IVDU)
○ Children with congenital heart disease
○ Anyone with prosthetic heart valves or pacemakers
○ Those with bad dental hygiene
More common in males
Fever + new murmur = endocarditis until proven otherwise. Any fever lasting >1wk
in those known to be at risk must prompt blood cultures.
What are the most common bacterium that can cause Infective Endocarditis
Developing world/Dentist - Viridins group strep
Surgery/Proestetic valve - Stap Epidermis
Developed world/IVDU - Staph Aureus - most common
Candida (Fungal) - infected long lines / hickman lines in patient with immunocompromise - also for new valves
More rarely, pseudomonas, pneumococcus, aspergillus - patients with immunocompromise
What infective endocarditis bacteria is likely to be seen in
a) IVDU
b) Surgical procedure
c) Dental procedure/Dental infection
a) Staph Aureus
b) Coagulase negative stapylococci (eg staph Epidermidis
c) α-haemolytic streptococci, (Strep viridans)
What are some risk factors for getting infective endocarditis?
- Previous Rheumatic heart disease (rare in the western world)
- Age related valvular degeneration
- Prosthetic valve (both mechanical and bioprostheses)
IV drug use
Fever + new murmur = endocarditis until proven otherwise. Any fever lasting >1wk
in those known to be at risk must prompt blood cultures.
What heart valve is most commonly affected in infective endocarditis?
The tricuspid valve is the first heart valve to be encountered after blood has returned from the
systemic circulation, so bacterial seeding is most common here – the tricuspid is the primary effected
valve in ~50% of patients, with the mitral and aortic being less common (both at ~20%), although
there is often a mixed picture.
What is the pathophysiology behind Infective endocarditis? What happens it in and how can it cause the complications it does?
The damage of the endocardium leads to thrombi formation, made of platelets and fibrin, it often causes in areas of high haedynamic pressure where there are shearing forces - aka around valves
Bacteria are able to colonise the thrombi, creating a Vegetation leading to Infective endocarditis.
These infected thrombi can become large enough to form an obstruction, or they may also break off to form emboli.
This emboli can go to affect CNS, lungs, spleen, kidney
Fever + new murmur = endocarditis until proven otherwise. Any fever lasting >1wk
in those known to be at risk must prompt blood cultures.
What are some key presentations of someone with Infective endocarditis?
What is sometimes the first sign of IE?
Depends on site where embolism is affecting, so potentially could have - Stroke, PE, Kidney dysfunction
Valve dysfunction, new murmurs
General septic signs, like Fever, sweating, malaise, Rigors, splenomegaly, clubbing
A INR that has shot up international normalised ratio, measure of blood clotting time)
Niche presentations seen in Infective endocarditis - what are
a) Janeways lesions
b)Roth spot
c) Osler’s Nodes
d) Splinter haemorrages?
a) Janeways lesions small, painless, red-brown lesions that appear on the palms of the hands and soles of the feet.
b)Roth spot - Roth spots are red-centered retinal hemorrhages, usually found in the peripheral retina.
c) Osler’s Nodes - small, tender, raised bumps on the hands and feet.
d) Splinter haemorrhages are tiny linear or needle-like streaks of blood that can be seen under the fingernails or toenails
Taken from Prof Chico IE Lecture, 2023
What is the Duke criteria? How would you use it?
- how you diagnose Infective Endocarditis - has two criteria, major and minor
Major (2)
- Pathogen grown from 2 separate blood cultures
-Evidence of endocarditis on echo, or new valve leak
Minor (5)
a) Predisposition ie Cardiac lesion, IVDU
b) Positive blood cultures that don’t meet major criteria
c) Fever
d) Immune phenomena - glomerulonephritis, Roth spot ,Osler’s nodes
e) Vascular phenomena - aka major arterial emboli, septic pulmonary infarcts, conjunctival/intracranial haemorrhages, Janeway lesions
PPFIV
Definite IE
2 majors, or 1 major and 3 minors, or all 5 minors
Possible IE
1 major and 1 minor
3 minor
What are some investigations you can do for suspected Infective endocarditis?
How should you take blood for IE?
Transoesophageal Echo (TOE) - DIAGNOSTIC
○ Generally safe but risk of perforation or aspiration
○ Easiest if ventilated (but never ventilate just for TOE)
* Transthoracic echo (TTE), safer, but lower sensitivity
- ECG
*Urinalysis
*FBC - look for elevated leukocytes, or elevated CRP (C Reactive protein),
Increased INR - CXR – cardiomegaly
- Blood cultures - take 3 cultures, from 3 different sites, at different times
What are the main lines of management for infective endocarditis? When would surgery be appropiate?
Antimicrobials!!
Treat complications, aka arrhythmias, Heart failure, heart block, stroke
Surgery - if can’t be cured with anbtx, there are complications, to remove infected devices, or replace valves Also can use surgery to remove large vegetations before they embolise
What antibiotics would you give for infective endocarditis in
a) Acute presentation
b) Subacute presentation
c) resistant organism, or prostetic valve
d) penicillin allergy
Acute presentation – flucloxacillin, gentamycin
Subacute presentation – benzylpenicillin, gentamycin
Prosethetic valve / resistant organism – triple therapy of vancomycin, gentamycin and rifampicin
In cases of penicillin allergy, then vancomycin (a glycopeptide – other example is teicoplanin) is the usual substitute.
Fever + new murmur = endocarditis until proven otherwise. Any fever lasting >1wk
in those known to be at risk must prompt blood cultures.
Antibiotics for Infective endocarditis
What give for an IE infection caused by Staphs,
in
a) native valve
b) Prosthetic valve
Staphs—native valve: flucloxacillin - If allergic or MRSA: vancomycin + rifampicin.
Staphs—prosthetic valves: flucloxacillin + rifampicin + gentamicin
Antibiotics for infective endocarditis]
what do you give for an IE infection caused by
Streps
Enterococci
- Streps—fully sensitive to penicillin: benzylpenicillin, or if less sensitive: benzylpenicillin + gentamicin
- Enterococci: amoxicillin + gentamicin, if penicillin allergic = vancomycin + gentamicin
Describe what heart failure is.
In what two ways can it happen?
When the heart can’t supply enough blood to meet the body’s demands
Either by systolic Heart failure, where heart’s ventricles can’t pump blood hard enough during systole (not squeezing enough(
or by Diastolic heart failure, where or not enough blood fills the ventricles during diastole (not filling enough) (reduced preload)
What happens in both systolic and diastolic heart failiure? What is this known as?
Blood backs up into the lungs, causing congestion or fluid build-up,
which is why it’s also often known as congestive heart failure, or just CHF.
What is systolic heart failiure?
What are it’s main causes?
Ejection fraction <40% (SV/EDV)
Caused by
IHD
MI
Hypertension
Cardiomyopathy
What is diastolic heart failure? What are its made causes?
Inability to relax and fill
There is reduced preload because there is abnormal filling of the LV
Ejection fraction >50%
Caused by
Constrictive pericarditis
Cardiac tamponade
Hypertension
What is a normal ejection fraction?
What ejection fraction would indicate systolic heart failure?
50-70% of blood in the ventricles being pumped out the heart in ventricular systole.
40% or under would indicate systolic heart failure 40% (SV/EDV)
What is it called when someone has RS heart failure and LS heart failure?
Biventricular heart failiure
How is Left sided heart failure often caused - Diastolic failure or systolic failure? How can ischaemic heart disease cause this?
What will happen as a result?
Often by systolic HF, as damage to the myocardium means heart can’t contract as forcefully and pumped blood as efficiently
Ischemic heart disease caused by coronary artery atherosclerosis, or plaque buildup, is the most common cause.
In this case, less blood and oxygen gets through the coronary artery to the heart tissue, which damages the myocardium.
===> In severe cases MI lead to scar tissue, which would also lead to this
What type of heart failure does long standing Hypertension lead to? How does long standing hypertension cause heart failure?
Because systemic hypertension makes it harder for the left ventricle to pump blood out into that systemic circulation.
To compensate, the left ventricle goes under hypertrophy so that the ventricle can contract with more force.
The increase in muscle mass means that there is a greater demand for oxygen and, to make things even worse, the coronaries get squeezed down by the this extra muscle so that even less blood’s delivered to the tissue.
Leads to more demand and reduced supply means that some of the ventricular muscle starts have weaker contractions—leading to systolic failure.
taken from osmosis video
What are the signs of left sided heart failure?
Signs:
Cardiomegaly (displaced apex beat)
Pulmonary Oedema
3rd and 4th heart sounds
Pleural effusion
Crepitations in lung bases
Tachycardia
Reduced BP
Cool peripheries
Heart murmur
What type of heart failure does Dilated cardiomyopathy lead to? How does dilated cardiomyopathy cause heart failure?
Left sided heart failure
Cardiomyopathy is a chronic disease of the heart muscle which causes the heart to become weak and enlarged., as it attempts to increase preload and stroke volume via Frank-starling law
This can lead to heart failure, where the heart is unable to effectively pump enough blood to meet the body’s needs.
How can long standing hypertension lead to diastolic heart failure?
The hypertrophy that is created by hypertension is concentric, which means that the new sarcomeres are generated in parallel with existing ones.
This means that heart muscle encroaches on the ventricular chamber space, resulting in less room for blood in there -> Can’t fill up as much
==> Therefore contributes to systolic but can also cause diastolic heart failure
Define cardiomyopathy
Group of disease of myocardium that affect mechanical or electrical function of heart
Name some types of cardiomyopathy
Hypertrophic cardiomyopathy (can be caused by hypertension, see card on it)
Dilated cardiomyopathy
Arrhythmogenic Cardiomyopathy
Restrictive cardiomyopathy
Outline the pathophysiology of dilated cardiomyopathy
What does it lead to?
Walls either normal or thin 🡪 weak contraction 🡪 less pumped out 🡪 biventricular congestive HF
Outline the pathophysiology of arrhythmogenic cardiomyopathy
Desmosome gene mutations Lead to arrhyhmias
Arrhythmogenic cardiomyopathy (ARVC/ALVC) –
Arrhythmia main feature of arrhythmogenic cardiomyopathy
Outline the pathophysiology of restrictive cardiomyopathy
Restrictive physiology – ventricles stiffer and less compliant 🡪 less CO 🡪 HF
What do the kidneys do when the heart fails to pump out enough blood?
What does this lead to in the heart, and later in other parts of the body?
decreases blood flow to the kidneys,
activates the renin-angiotensin-aldosterone system, ultimately causing fluid retention.
Which fills the heart a bit more during diastole and increases preload, which increases contraction strength again by the Frank Starling mechanism.
leads to fluid retention, aka oedema
How can left sided heart failure cause right sided heart failure?
LSHF leads to increased pulmonary blood pressure, due to fluid build up.
increased pulmonary blood pressure makes it harder for the right side to pump blood into.
In this case the heart failure would be biventricular, since both ventricles are affected.
What are some causes of Right sided heart failure?
Hypertension
Pulmonary stenosis
Lung disease (cor pulmonale)
Atrial/ventricular septal defects
How can Atrial and ventricular septal defects cause RS heart failure?
It allows blood to flow from the higher-pressure left side to the lower-pressure right side, which increases fluid volume on the right side
Eventually leads to concentric hypertrophy of the right ventricle, making it more prone to ischemia— (Systolic Failure)
….and have a smaller volume and become less compliant - (Diastolic failure)
What is Cor pulmonale? What are some of its causes?
Right sided heart failure caused by chronic arterial pulmonary hypertension, due to lung diseases, Pulmonary vascular disorders, neuromuscular and skeletal diseases
How can lung disease cause right sided heart failure? (cor pulmonale)
Hypoxia due to the disease causes Pulmonary arterioles constrict 🡪 increase pulmonary BP 🡪 harder for RV to pump against 🡪 hypertrophy and failure
Where does blood get backed up to in
a)Left sided heart failure
b) right sided heart failure?
a) - the lungs
b) the systemic veins - leading to Systemic vein congestion - *think raised JVP
blood backing up into the systemic veins in
a) Jugular vein
b) liver and spleen
c) peritoneum
d) interstitial soft tissue space - legs and sacrum
leads to what signs/symptoms in right sided heart failure?
Blood back up into jugular vein Raised JVP, – JVP distension -
b) leads to Hepatomegaly and Splenomegaly (Hepatosplenomegaly)- In extreme cases and lead to cirrhosis of liver, known as cardiac cirrhosis
c) Fluid build up in peritoneum leads to Ascites and weight gain
d) leads to Pitting oedema – sacral/leg oedema in bed-bound patients which causes a “pit” when pressed
What are the signs/symptoms of Right hand sided heart failure?
Raised JVP – JVP distension
Hepatomegaly/Splenomegaly
Pitting oedema – sacral/leg oedema in bed-bound patients which causes a “pit” when pressed
Ascites
Weight gain (fluid)
What are the specific breath related symptoms that you see in heart failure (exam fodder)
paroxysmal nocturnal dyspnoea
orthopnoea
Exertional dyspnoea
What are the 3 cardinal signs of Heart failure?
shortness of breath (and must say specifically at least one of; paroxysmal
nocturnal dyspnoea, orthopnoea),
Ankle swelling,
Fatigue
What are some symptoms of left sided heart failure?
Exertional dyspnoea
Fatigue
Weight loss
Paroxysmal nocturnal dyspnoea – attacks of severe SOB and coughing at night
Nocturnal cough – pink, frothy sputum
Orthopnoea – dyspnoea (SOB) that occurs when lying down
What are some signs of left sided heart failure?
think about what it backs up into! (left side backs up into lungs)
Cardiomegaly (displaced apex beat)
Pulmonary Oedema
3rd and 4th heart sounds
Pleural effusion
Crepitations in lung bases
Tachycardia
Reduced BP
Cool peripheries
Heart murmur
name some investigations for suspected heart failure
ECG
Chest X ray
BNP B-type Natriuretic Peptide levels
Echocardiogram
What could you see on an ECG in someone with heart failure?
Should be performed on all suspected heart failure patients
May indicate the underlying cause of the heart failure such as;
Myocardial infarction/ischemia
Bundle Branch Block
Ventricular hypertrophy
Pericardial disease
Arrhythmias
Signs of previous MI - pathological Q waves
A normal ECG makes heart failure unlikely (sensitivity 89%)
taken from almostadoctor
What could a chest Xray show for someone with heart failure
ABCDE
Recommended for all suspected HF patients
Alveolar oedema - seen in Bat wing shadowing
Kerley B Lines interstitial oedema
Cardiomegaly
Dilated upper lobe vessels of lungs (prominent upper lobe veins)
Effusions (pleural)
A normal CXR does not exclude the possibility of Heart Failure
What are Kerley B lines (seen on chest xray for heart failure)
thickened, horizontal lines that radiate from the costophrenic angle - they are the interlobular septa (that separate lobes of the lungs) that have become filled with fluid
Basically oedema within the interlobular septa - interstitial oedema
What is BNP? Why is it increased in heart failure
B-type Natriuretic Peptide (BNP) are peptides that cause natriuresis, diuresis and vasodilation.
HF - released in response to increased pressure on heart -
BNP signals to the body that it needs to reduce the amount of fluid in the body, and help reduce the strain on the heart. ==
They are the body’s “natural defence” against hypervolaemia
A marker of heart failure
Released when the myocardial walls are under stress
Levels directly correlated to ventricular wall stress and severity of heart failure
RELEASED FROM THE VENTRICLES
What is the diagnostic test for heart failure? What uses does it have?
ECHOCARDIOGRAM
Can confirm the diagnosis
Can calculate the ejection fraction, ventricular wall thickness etc
An ejection fraction (EF) of <40% strongly indicated heart failure
EF of 41-49% is not diagnostic, but suggestive of heart failure
Can confirm any underlying structural abnormalities – such as valve disease
Helps to stratify the type of HF present and therefore guides management
What are the classifications seen in the New York Heart Association, when gauging the extent of heart failure? seen in OHCM
BASED ON LIMITATIONS
Class I: No limitation (Asymptomatic)
Class II: Slight limitation (mild HF)
Class III: Marked limitation (Symptomatically
moderate HF)
Class IV: Inability to carry out any physical
activity without discomfort (symptomatically
severe HF
1- Nothing, 2 -Mild, 3 - Moderate, 4 - Severe
name some non pharmalogical interventions to help treat heart failure
Exercise more
Reduced salt intake and processed foods, monitor weigh
Fluid restriction in severe cases
Reduce alcohol, stop smoking
Get flu vaccination
What medication can you specifically give for acute heart failure that is causing symptoms? (aka acute on chronic heart failure)
A diuretic, like furosemide
What is the first line treatment for those with heart failure and preserved ejection fraction (HFPEF)
A diuretic, like furosemide
The following flashcards will be asking about heart failure medication for when there is a reduced ejection fraction
Heart failure medication 1:What is the first medications you should give in patients with heart failure with reduced ejection fraction?
- an ACE inhibitor, like Ramipril, and Beta blockers, like Bisoprolol
Start low, progress slow! - monitor BP and heart rate
ABAL
(can consider giving an Angiotensin 2 receptor blocker eg Candesartan if intolerant of ACE-i)
Heart failure medication, with reduced
ejection fraction 2: After ACE inhibitors, and Beta blockers what other medications can you give?
A mineralocorticoid receptor antagonist - eg Spironolactone
Heart failure medication 3 - After ACE inhibitors and beta blockers , what other medications can you give?
K+ sparing diuretic, like Spironolactone - Aldosterone receptor antagonist
ABAL
Also a drug like Digoxin - good for arrhythmias and AF, and helps symptoms of LVSD (Left Ventricular Systolic Dysfunction.)
—> Helps strengthen heart muscle contractions
What drugs used in heart failure can have the side effect of Gynaecomastia?
Digoxin - used AF CAN ALSO CAUSE HYPERKALAEMIA
Spironolactone - an aldosterone receptor antagonist
(Not used in heart failure, but anabolic steroids and antipsychotics that inhibit dopamine and therefore nothing to restrict prolactin can also cause Gynaecomastia)
Cardiac Pharmacology: What are the main clinical indications for Angiotensin Converting Enzyme Inhibitors? Give some common examples of these
Hypertension
Heart failure
Diabetic nephropathy
eg RAMIPRIL, ENALAPRIL, PERINDOPRIL, TRANDOLAPRIL
Cardiac Pharmacology - what are the main adverse effects of Angiotensin converting enzyme inhibitors?
Think - Due to reduced angiotensin II formation!! (duh)
a. Hypotension b. Acute renal failure c. Hyperkalaemia d. Teratogenic effects in pregnancy
Also due to increased Kinin production
a. Cough b. Rash c. Anaphylactoid reactions
Cardiac Pharmacology: What are the main clinical indications for Angiotensin II receptor blockers? Give some common examples of these?
Hypertension
Diabetic nephropathy
Heart failure (when ACE-I contraindicated)
eg CANDESARTAIN, VALSARTAIN, LOSARTAN
Cardiac Pharmacology - what are the main adverse effects of Angiotensin II receptor blockers? When is it contraindicated?
Symptomatic hypotension (especially volume deplete patients)
Hyperkalaemia
Potential for renal dysfunction
Rash
Angio-oedema
Contraindicated in pregnancy (aka not safe for pregnancy)
Generally very well tolerated
Cardiac Pharmacology: What are the main clinical indications for Calcium Channel blockers? Give some common examples of these?
Hypertension
Ischaemic heart disease (IHD) – angina
Arrhythmia (tachycardia)
eg AMLODOPINE, FELODIPINE, VERAPAMIL, DILTIAZEM
Cardiac Pharmacology: What are the main clinical indications for Beta-adrenoceptor blockers? Give some common examples of these?
Ischaemic heart disease (IHD) – angina
Heart failure
Arrhythmia
Hypertension
eg BISOPROLOL, PROPRANOLOL, ATENOLOL, NADOLOL
What is a key drug to be avoided in heart failure
Calcium channels blockers, with the exception of Amlodipine, are generally avoided in heart failure, and verapamil in particular can worsen heart failure.
Some Beta blockers are B1 selective, while others are non-selective, meaning they bind to and block either B1 or B2 receptors. Name some B1 selective drugs, and some non selective drugs, and the intermediate between the two.
B1 selective - Metoprolol, Bisoprolol
in the middle - Atenolol
B1/B2 non selective - Propranolol, nadol
The term “cardioselective” is often used to imply β-1 selectivity
This is a misnomer since up to 40% of cardiac β-adrenoceptors are β-2
What are the main adverse effects of Beta-adrenoceptor blockers?
Fatigue
Headache
Sleep disturbance/nightmares
Bradycardia
Hypotension
Cold peripheries
Erectile dysfunction
Worsening of: Asthma (may be severe) or COPD
PVD – Claudication or Raynaud’s
Heart failure – if given in standard dose or acutely
Cardiac Pharmacology: What are the main clinical indications for diuretics?
What are the 4 classes of Diuretics, and where do they act?
Hypertension
Heart failure
Classes
Thiazides and related drugs (act on distal tubule)
Loop diuretics (act on loop of Henle)
Potassium-sparing diuretics
Aldosterone antagonists
Cardiac Pharmacology - give some examples of
a) Thiazide and related diuretics
b) Loop diuretics
c) Potassium sparing diuretics
a) Bendroflumethiazide, hydrochlorothiazide
b) Furosemide, Bumetanide
c) Spironolactone Amiloride
Cardiac pharmacology - name some main adverse effects on Diuretics, and if appropriate, give name the main class of diuretic responsible for it.
Hypovolaemia and hypotension - Mainly caused by Loop diuretics eg furosemide
Low serum potassium (hypokalaemia)
Low serum sodium (hyponatraemia)
Low serum magnesium (hypomagnesaemia)
Low serum calcium (hypocalcaemia)
Raised uric acid (hyperuricaemia – gout)
Erectile dysfunction and Impaired glucose tolerance - Mainly thiazides eg Bendroflumethiazide,
spironolactone can cause gynecomastia
Normal physiology - what is Atrial natriuretic peptide and B-(Brain) natriuretic peptide? When is it released and what does it do?
Released from atria and ventricles.
Released by stretching of atrial and ventricular muscle cells, in Raised atrial or ventricular pressures or volume overload
Actions
Increase renal excretion of sodium (natriuresis) and water (diuresis)
Relax vascular smooth muscle (except efferent arterioles of renal glomeruli)
Increased vascular permeability
Inhibit the release or actions of:
Aldosterone, angiotensin II, endothelin, anti-diuretic hormone (ADH)
Counter-regulatory system to the renin-angiotensin system
Cardiac pharmacology - what do nitrates do, and when are they used?
They are Arterial and venous dilators
Reduction of preload and afterload
Lower BP
Ischaemic heart disease (angina)
Heart failure
MI
Cardiac pharmacology - give some examples of nitrates, and some adverse effects of them
Isosorbide mononitrate
GTN Spray
GTN infusion
GTN = Glyceryl Trinitrate
Main adverse effects: Headache; GTN syncope (spray)
What is the main adverse effect of Caclium channel blockers?
Ankle oedema (Augmented drug reaction)
Heart sounds - what is S1 heart sound made by? Why does it happen? Is it normal or pathological?
S1 - CLOSING OF AV VALES, START OF SYSTOLIC CONTRACTION - STOPS BLOOD GOING OUT OF VENTRICLES AND BACK INOT ATRIA
NORMAL
Heart sounds - what is S2 heart sound made by? Why does it happen? Is it normal or pathological?
S2 - CLOSING OF THE SEMI LUNAR VALVES , WHEN SYSTOLE IS CONMPLETE - STOPS BLOOD FLOW BACK INTO VENTIRICLES
NORMAL
Heart sounds - what is S3 heart sound made by? Why does it happen?
S3 - HEARD 0.1S AFTER S2 SOUND SUBTLE - CAUSED BY THE RAPID VENTRICLE FILLING, MEANING THE CHORDI TENDONAE EXTEND TO FULL STRETCH AND TWANG
When is S3 normal, and when is it pathological?
NORMAL IN YOUNG HEALTHY PATIENTS, heart fills and stretches easily
CAN INDICATE HEART FAILURE IN OLDER PATIENTS, AS CHORDI TENODNAE ARE STIFF A WEAK - SO REACH STRETCHING LIMIT MUCH QUICKER THAN USUAL
eg old person bending over, and their hamstrings quickly tighten as they reach limit of stretch
Lub DeDub
Heart sounds - what is S4 heart sound made by? Why does it happen? When does it happen? Is it normal or pathological?
S4 - HEARD DIRECTLY BEOFRE S1 - INDICATES A STIFF AND HYPERTROPHIC VENTRICLE - SOUND CAUSES BY TURBULENT FLOW OF AN ATRIA, THAT IS CONTRACTING AGAINST THE VENTRICLE THAT IS NOT RELAXED/NON COMPLIANT ===> TURBULENT FLOW
Where is the best place to listen to heart sounds?
ERB’s POINT - 3rd Intercostal space, left sternal boarder - best place to listen to heart sounds S1-S4
What will happen to a heart chamber that is pushing against a stenotic valve? Give an example.
If heart chamber is pushing against stenotic valve - has to work a lot harder- aka will undergo hypertrophy
AKA if mitral valve is stenotic, will get left atrial hypertrophy
Aortic stenosis = left ventricular hypertrophy
What will happen to a heart chamber that is ejecting blood into another chamber via an incompetent/regurgitive valve? Give an example
In a leaky valve, blood will reenter back to the chamber it came from, stretching the muscle in it- leading to a dilated chamber
eg Aortic Regurgitation - blood flows back into left ventricle after systole when it shouldn’t leads to left ventricular dilation
What is the most common valvular heart disease?
Aortic Stenosis
What is aortic stenosis?
It is the narrowing and stiffening of the aortic valve - specifically of the 3 cusps that form it.
It is progressive
Outline some of the key epidemology of aortic valve disease
Most common valve disease
Presenting Patients are normally in their 70s or over
What are the common causes of Aortic stenosis?
Calcification of the aortic valve over time
Congenital issues - aka having a bicuspid aortic valve (2 cusps) not 3 - These are far more prone to calcification
Rheumatic fever is a rare cause
What presentation would make you think of aortic stenosis, as a doctor?
What is the classic triad seen in aortic stenosis?
Think of it in any old person with the classic triad of:
- Syncope (can be on exertion)
- Angina
-Dyspnoea
Also think of it in heart failure
What is a specific heart sound that you could hear in a patient with aortic stenosis?
causing an ejection systolic murmur - high pitched due to high velocity, turbulent blood flow
Will radiate up to carotid as turbulence radiates up to the neck
Murmur is also known as crescendo decrescendo - louder than quieter
Sounds like a whoosh
What signs can be seen on investigation of someone with aortic stenosis?
What would you see on xray in aortic stenosis
- Slow rising (pulsus tardus) and weak (pulsus parvus) carotid pulse
- loud ejection systolic murmur at the aortic area, radiating to both carotid arteries - can have a crescendo-decrescendo character
- Soft or absent S2 sound - as A2 (aortic sound) is far quieter
- Can also observe pathological S4 korsakoff heart sound
On Xray - Cardiomegaly, dilated ascending aorta,
pulmonary oedema, calcification of aortic valve
What is the management for aortic stenosis
- Surgical
○ Aortic valve replacement – in symptomatic patients as onset of symptoms associated with 75% mortality at 3 years
○ If not medically fit for surgery, then Transcatheter Aortic Valve Implantation (TAVI) with a balloon expandable stent Balloon valvoplasty- General
○ Dental hygiene/care – risk of infective endocarditis
○ IE prophylaxis (IPC) in dental procedures
- General
What is mitral valve stenosis?
Mitral leaflets fuse together, leading to obstruction of inflow to left ventricle = prevents proper filling during diastole, due to narrowing of mitral valve
(Normal mitral valve orifice is 4-6cm^2)
Where/when is mitral valve stenosis most common?
More common in females, 40-50 years old
What are the most common causes of mitral valve stenosis?
Rheumatic heart disease
rheumatic fever from group A beta-haemolytic strep e.g. s. pyogenes
Infective endocarditis
Congenital deformation of mitral valve
Carcinoid tumours
What puts you at risk to getting mitral valve stenosis?
- History of rheumatic fever
- Untreated streptococcus infections
What pathology does having mitral valve stenosis lead to? What is the pathophysiology behind this?
LA hypertrophy = PULMONARY HYPERTENSION, ARRHYTHMIAS
Thickening and immobility of valve leads to obstruction of blood flow from LA to LV
===> increased LA pressure, which can eventually lead to pulmonary hypertension and right heart dysfunction
High Pressure in left atrium can also lead to Atrial fibrillation, which can lead to further thrombi forming, can cause things like stroke
pulmonary hypertension can pulmonary oedema
What is a specific heart sound you can hear in mitral valve stenosis?
Mid diastolic low pitched, rumbling murmur
This is a murmur after S2, due to the low velocity of the blood going through it into the ventricle
also A Loud S1 (Due to Thick mitral valve suddenly forcefully shutting)
eg LUB! DUBdurrrr see picture
What are some signs of mitral valve stenosis that can be detected on examination
Malar flushes on cheek –decreased CO can cause vasoconstriction which results in pinkish-purple patches on the cheeks
Loud first heart sound due to increased pressure in LA, with a tapping apex beat
loud P2, due to pulmonary Hypertension
Diastolic murmur – heard when blood flows over a valve
How can you position the patient in order to give you the best possible chance of hearing mitral stenosis?
Get them to lie on their left hand side
What are some symptoms of mitral valve stenosis?
Think what MVS will lead to, and the symptoms of these!
MVS - leads to LA hypertension, so can cause pulmonary hypertension/RSHF!
* Progressive exertional dyspnoea
* Haemoptysis – coughing up blood due to rupture of bronchial vessels due to elevated pulmonary pressure
* Right HF
○ Fatigue
○ Weakness
○ Abdominal/lower leg swelling
* Palpitations – due to AF
* Chest pain
What tests would you do for suspected mitral valve stenosis? What results would you see?
- Echocardiogram - can see left atrial enlargement , thick and calcified mitral valve
- CXR – LA enlargement, pulmonary hypertension and sometimes a calcified mitral valve
- ECG – AF and LA enlargement
What is the treatment for someone with mitral valve stenosis?
Control symptoms that it has caused:
- Rate control if patient has AF – beta blockers, digoxin
-
Anticoagulation with warfarin for AF patients to prevent clot formation and embolisation
Diuretics for heart failure e.g. furosemide - Percutaneous mitral balloon valvotomy – access to mitral valve obtained via catheterisation through the femoral vein, RA and interatrial septum and a balloon is inflated to open the orifice
What is aortic regurgitation?
Aortic regurgitation (AR) occurs when there is a backflow of blood from the aorta into the left ventricle during ventricular diastole.
taken from geekymedics
What are the most common causes of aortic regurgitation?
either acute or chronic:
* Congenital bicuspid aortic valve - chronic
* Rheumatic heart disease (rheumatic fever) - chronic
Connective tissue diseases (e.g. Marfan’s syndrome)
- Infective endocarditis - acute
- Chest trauma - acute
- Aortic dissection - acute (inner layer of aorta tears, so blood flows between layers of wall, forcing it apart
What does aortic regurgitation lead to?
It leads to a combined volume and pressure overload in the left ventricles
What position can you put the patient in in order to give you the nest chance of hearing aortic regurgitation on auscultation?
Get them to sit up, lead forward, breathe out and hold it, then listen
What specific heart sound can you hear in aortic regurgitation?
an early diastolic, soft murmur - Very subtle!
due to blood flowing straight back into left ventricle from aorta during diastole ==> because of this, also associated with a collapsing pulse
What signs of aortic regurgitation can be picked up on examination?
WATERHAMMER PULSE
- Early diastolic murmur due to backflow - heard at left sternal edge 4th IC space
- Ejection systolic murmur due to more volume in left ventricle when it contracts
Wide pulse pressure
Quincke’s Sign
De Musset’s sign
Muller’s Sign
What is a waterhammer pulse, and what is it also known as? How would you look for one?
Water hammer pulse/collapsing pulse
- get Pt to sit down and lie back, and raise up arm, Grab Muscular part of forearm, and will feel a tapping pulse, as blood that is pumped into arm during systole is emptied into heart during diastole
Can be seen in Aortic regurgitation
Aortic Regurgiation sign’s - what is
a) Quincke’s Sign
b) De Musset’s sign
c) Muller’s Sign
- Quincke’s sign – capillary pulsation in nail beds
- De Musset’s sign – head nodding with each heart beat
Muller’s sign – visible pulsations of uvula
c for capillary = quinCke
What symptoms would someone with aortic valve regurgitation experience?
- Exertional dyspnoea
- Orthopnoea - struggling to breathe lying down
- Paroxysmal nocturnal dyspnoea - sudden onset of difficulty breathing at night
- Palpitations
- Angina
Syncope
What investigations would you carry out for aortic valve regurgitation?
- Echocardiogram
- ECG – shows evidence of LVH
- CXR - shows a large heart (cardiomegaly) and occasional dilatation of the ascending aorta
Cardiac MRI
What are the treatment options for aortic regurgitation?
- Vasodilators – ACE inhibitors e.g. Ramiprils only if symptomatic or hypertension
- Surgical – replace valve before LV dysfunction
What is mitral valve regurgitation?
Imperfect closure of mitral valve during systole, leads to back flow into left atria
Name some of the causes of mitral valve regurgiations
Degenerative mitral valve disease - most common cause in developed world
Also:
* Infective Endocarditis
* Ischaemic mitral valve
Dilated cardiomyopathy
Connective disorders, like Maarfans
In Developing world:
Rheumatic heart disease – from rheumatic fever
What are some risk factors for mitral valve disease?
Risk Factors
* Female
* Lower BMI
* Advanced age
* Renal dysfunction
* Previous MI
What is the pathophysiology that is behind the issues caused by mitral valve regurgitation?
- Pure volume overload due to leakage from LV into LA 🡪LA dilatation
- Compensatory mechanisms:
○ LA enlargement
○ LV hypertrophy – since LV must put in same effort to pump less blood
○ Increased contractility
○ Progressive LA dilatation and RV dysfunction due to pulmonary hypertension
○ Progressive LV volume overload leads to dilatation and progressive HF
○ LA enlargement can Lead to AF
What are some symptoms of mitral valve reguritation?
- Exertional dyspnoea
- Fatigue and lethargy
- Palpitations
- Right sided HF and can lead to congestive heart failure
Symptoms of any heart valve defect
What specific heart sound would you hear in someone with mitral regurgitaiton?
Get a Pan systolic murmur - murmur that is present throught the systolic period - due to blood following back into the atria during ventricular contraction
It’s high pitched and whistling, due to the high velocity of blood flow back through the leak vale, from ventricular contraction
What are some signs that can be detected on examination of mitral valve disease?
- Collapsing pulse with wide pulse pressure
- Hyperdynamic and displaced apex beat
○ Soft S1
Mitral stenosis - Mid diastolic low pitched murmur, after S2
Mitral regurgitation = PAN SYSTOLIC MURMUR - Due to blood going back into atria - High pitched and whistling, due to high velocity of blood going back into atria - radiates to the axilla
Any sound produced by the mitral valve will radiate to the axilla
What investigations would you carry out for suspected mitral valve regurgitation?
- ECG – P Mitrale – ‘bifid’ (two-peaks) P waves due to atrial hypertrophy
- Trans-Oesophageal Echocardiogram – TOE – used to asses the level of valve damage, to check if suitable for valve repair / replacement
- Doppler-Echo – assesses the site and size of the regurgitant jet
What are The most common valve dysfunctions secondary to heart failure?
functional mitral and tricuspid regurgitations.
This is because the enlarged ventricles cause an incomplete seal at the valves during diastole.
What is Hypertension? What values does the WHO classify it as?
High Blood pressure!
WHO classification – 140/90 mmHg on at least two readings on separate occasions
What is the prevalence of hypertension in England for
a) Men
b) Women
The prevalence of high blood pressure in 2015 was reported as 31% among men and 26% among women, affecting more than 1 in 4 adults.
How many people have hypertension worldwide?
What percentage of adult black Africans have hypertension?
1.13 billion people have hypertension worldwide (defined as systolic blood pressure [BP] ≥140 mmHg and diastolic BP ≥90 mmHg)
- Hypertension is more common in black Africans – 40-45% of adults
What % of hypertension cases are primary (essential)? What about Secondary?
90-95% primary, 5-10% secondary
What are some causes of primary hypertension?
It has multifactorial aetiology
Genetic factors – can run in families 40%-60% have a genetic component
Foetal factors – low birth weight is associated with hypertension
Obesity
High alcohol Alcohol intake
Insulin intolerance
Lack of physical activity
Metabolic Syndrome X cluster of conditions, such as high insulin levels, glucose intolerance, low levels of HDLs, central obesity
What are some risk factors for developing hypertension
- Family history
- Old age
- Low birthweight
- Male
- Afro-Caribbean’s
- Unhealthy diet
- Lack of physical activity
- Obesity
What are some main causes of secondary hypertension?
○ Renal e.g. CKD
○ Endocrine e.g. Conn’s syndrome, acromegaly, Cushing’s syndrome
○ Coarctation of the aorta
○ Pre-eclampsia occurring during third trimester of pregnancy
Outline the pathophysiology behind some of the issues that hypertension does to the body.
Hypertension - Causes arteries to common less compliant, and narrowing of the lumen
Can lead to Hyaline arteriosclerosis, which is protein deposition in the arterial wall,
Lead to atherosclerosis and aneurysms forming - stroke
Endothelial damage = CAD, ACS
What are the main symptoms of high blood pressure?
Asymptomatic – except in malignant hypertension
May have the occasional general headache although the reliability of this as a symptom is disputed
How do you measure blood pressure if you suspect hypertension? What are the two types of BP monitoring you can get a patient to do at home?
Take BP reading, and Repeat BP in the other arm
* Repeat again at the end of the consultation
*If it remains high, then arrange home BP monitoring; either:
Ambulatory BP monitoring (ABPM) – the patient is fitted with a BP recording device, which takes their BP every hour (or more) throughout a 24 hour period. -> tell them to keep doing their daily activities
Home blood pressure monitoring (HBPM) –
Ask the patient to keep a diary of their BP:
* Twice daily
* For 7 days
* Take two consecutive readings and record the lowest
* Discard the first day and take an average of the rest of the readings at a follow-up appointment
What other way can you look for signs of hypertension, that isn’t taking a BP reading?
What sort of things would you see?
Look at retina!
- Cotton wool spots - damage to nerve fibres
- Silver/Copper wiring - walls of the arterioles become sclerosed causing increased reflection of the light.
- Hard exudates leaking lipids into the retina.
- Papilledema is caused by ischaemia to the optic nerve resulting in optic nerve swelling (oedema) and blurring of the disc margin
- Retinal haemorrhages = releasing blood into the retina.
taken from zerotofinals
If you diagnose a patient for hypertension, then what tests should you organise doing next?
- Urinalysis to check for Kidney damage (Proteins/blood in wee, Albumin to creatine ratio)
- ECG/Echo for LV hypertrophy
- Fundoscopy for retina damage
- Bloods - Serum creatine, eGFR, Glucose (Hba1c)
- Take clinical history
Lipid Profile and QRISK
What are some complications of hypertension, if left untreated?
- Cardiac - MI, AAA, Atherosclorosis, AF, HF
- Stroke
- Renal failure
Eye defects
What non medicinal treatment can you give to someone to help with hypertension?
- Lifestyle changes
○ Smoking cessation
○ Low-fat diet + high consumption of fruit and vegetables
○ Reduce alcohol and salt intake
○ Increase exercise
Loss weight is obese
Hypertension medication - what is the first line treatment for someone who is NOT black, and under 55 years
ACE-Inhibitor e.g. Ramipril (or angiotensin receptor blocker e.g. candesartan if contraindicated e.g. due to cough)
What is the first line medication given to anyone with T2DM, regardless of age or race?
ACEi, eg Ramipril
Hypertension medicine - when would a Angiotensin receptor blocker be given? Give a example of one
eg Candesartan
It’s given instead of an ACE-inhibitor, if a ACE-i is contraindicated.
You give ACE-i to anyone who is younger than 55, or not Black afro Caribbean, or someone with Diabetes at any age .
Hypertension medication - what is the first line treatment for someone who is black, or over 55 years
calcium channel blocker e.g. amlodipine
Hypertension medication - what is the second line treatment for hypertension?
ACE-inhibitor + CCB
Or if afro Caribbean - CCB and ARB
Hypertension medication - what is the third line treatment for hypertension?
○ Third line = ACE-inhibitor + CCB + diuretics e.g. Bendroflumethiazide or furosemide
Cardiac pharmacology - what common antihypertensive medication can commonly cause peripheral oedema?
Calcium-channel blockers such as amlodipine commonly cause peripheral oedema
Hypertension medication - what is the fourth line treatment for treatment of hypertension?
Fourth line – ACE-inhibitor + beta blocker e.g. Bisoprolol + CCB + diuretics
What is a DVT?
What would a DVT in the upper body be suggestive of?
A DVT is a blood clot that forms in the deeper veins of the leg or pelvis, as opposed to the veins closer to the surface of the skin.
If these clots appear in other areas of the body, such as the arm, it can point to a more serious condition (eg Clotting disorder/Carcinoma) and usually requires long-term treatment or prevention.
Normal physiology - how does blood in superficial leg veins get to the heart? What helps propel blood back to the heart?
Blood from the superficial veins is transferred into the deeper veins, with the assistance of the skeletal muscle pump.
The muscles surrounding the vein contract, pushing the blood onward, and the valves in the vein restrict the backflow of liquid.
Normal physiology - outline the platelet plug and coagulation cascade. What are they both known as?
So vwf FACTOR bind to collagen, and starts off either intrinsic or extrinsic pathway =PLATELET PLUG, PRIMARY HOMEOSTASIS
Then is followed by secondary cascade is set off, which ends in FIBRONGEN BECOMING FIBRIN, leading to a mesh around the plug = SECONDARY HOMEOSTASIS
Intrinsic pathway , uncommon - 12 > 11 > 9 > 8 >10
Extrinsic pathway - more common 3 > 7 > 10
Both lead to common pathway, 10 > 5 > 2 > 1
Factor 2 is called Prothrombin, when activated becomes thrombin, Factor 1 is called fibrinogen activated becomes fibrin
10 is initiator of common pathway
Normal Physiology - What enzyme breaks down fibrin? What does it break fibrin down into?
Plasmin cuts up fibrin into pieces known as D-dimers.
What are the risk factors for developing a DVT?
ANYTHING THAT LEADS TO EXCESS CLOTTING!!
Age - Middle aged and over
Smoking
Immoniliity in legs - eg long flights, surgery, being bed bound
Pregnancy
Polycythaemia
Thrombophilia e.g. antiphospholipid syndrome, antithrombin deficiency, protein C or S deficiency Can be genetic
Having Virchow’s triad: hypercoagulability, venous stasis, endothelial damage
Where do most clots seen in DVT form? What is more dangerous - above or below knee clots?
deep veins of the leg start off at a spot situated just behind and above a venous valve.
Above knee is more dangerous, more likely to embolise
What are some signs of DVT?
- Unilateral swelling
- Oedema
- Tender and erythematous (red, flushed)
- Distention of superficial veins
- Phlegmasia cerulea dolens: occurs in a massive DVT, resulting in obstruction of venous and arterial outflow (rare). This leads to ischaemia and a blue and painful leg
What are some symptoms of DVT?
- Red, swollen leg (particularly calf)
- Tenderness
- Pitting oedema
- Fever
What are some investigations to do for suspected DVT?
Ultrasound scanning - cheap and quick - 90% accurate above leg, but only 50% accurate below leg
Venography - GOLD STANDARD - injection of a radio-opaque dye into the foot, allowing the path of the dye to be monitored as it travels up the leg
D-dimer levels -D-dimer, a breakdown product of fibrin, is also used to diagnose DVT. A negative test result rules out DVT, however a positive result does not necessarily mean the patient has the condition
Leg Measurement
Investigations for DVT - what leg measurement would be indicative of DVT? Where on the leg would you measure
This involves measuring the diameter of the calf on each leg, usually 10cm below the tibial tuberosity.
A difference of more than 3cm between the two legs can be an indication of DV
What is Wells Scoring, and when is it used?
The Wells score calculates the risk of DVT and determines how the patient is investigated and managed. Those with a score ≥ 2 are deemed high risk
taken from OHCM 9th edition
What kind of things are included in a Wells score?
Active Cancer = 1
Bedridden or recent major surgery = 1
Calf swelling >3cm compared to other leg = 1
Superficial (non varicose) veins present = 1
Entire leg swollen = 1
Tenderness along veins = 1
Pitting oedema of the affected leg - 1
immobility of affected leg - 1
Previous DVT - 1
Alternative diagnosis likely = -2 points
taken from OHCM 9th edition
What mamagement would you carry out if the Wells score was greater or equal 2? (DVT likely)
Duplex ultrasound of leg within 4 hours: this is diagnostic (offer a D-dimer if the scan is negative); if an ultrasound is not possible to arrange within 4 hours:
○ Perform a D-dimer AND
○ Offer interim anticoagulation for 24 hours (ideally in a form that can be easily continued) AND
○ Arrange the ultrasound for the following day
taken from OHCM 9th edition
What management would you carry out if the Wells score was lower or equal to 1? (DVT unlikely)
D-Dimer with a result available within 4 hours: if D-Dimer results cannot be obtained within 4 hours, offer interim anticoagulation until the result is available
○ If D-Dimer is raised: perform a duplex ultrasound within 4 hours
○ If D-Dimer is normal: a DVT is unlikely and alternative diagnoses should be considered
What anticoagulant would you give to treat DVT if
a) No renal impairment
b) Do have renal impairment
No renal impairment
§ Offer apixaban or rivaroxaban (Inhibits thrombin)
§ If neither suitable, offer one of:
□ LMWH for at least 5 days followed by dabigatran or
edoxaban (Inhibits thrombin)
Renal impairment (estimated creatinine clearance <15 ml/min)
§ Offer one of:
□ LMWH (Low Molecular Weight Heparin.)
□ Unfractionated heparin (UFH)
What preventive and non - medicinal treatment can you give in DVT?
- Compression stockings
- Frequent calf exercises during long periods of immobilisation
Prophylactic anticoagulation with LMWH e.g. in patients who have had surgery and will be immobilised for a long period of time
What are the complications of DVT?
- Pulmonary embolism: increased pressure in the vein can cause a part of the main clot to break free. Therefore, there is a risk of an embolism to the lungs. Pulmonary embolism can be diagnosed with a CT pulmonary angiogram or ventilation–perfusion (VQ) scan.
- Embolic stroke: seen in patients with atrial septal defect :, the clot may travel to the left atria and then the left ventricle. The clot can then embolise to any part of the body, including the brain causing an embolic stroke
- Post-thrombotic syndrome: this is a long term complication caused by chronic obstruction of venous blood, leading to venous hypertension, with pain, swelling, and ulceration
- Increased risk of bleeding: patients on anticoagulation are at risk of bleeding
- Phlegmasia cerulea dolens: occurs in a massive DVT, resulting in obstruction of venous and arterial outflow (rare). This leads to peripheral limb ischaemia and a blue and painful leg
What is a Pulmonary embolism?
Normally a complication of venous thromboembolism from elsewhere in the body.
The clot becomes dislodged, and goes via bloodstream to get dislodged in the lungs
Name some risk factors that can lead to a PE, based off the constituent parts of Virchow’s Triad
Virchow’s triad risk factors for PE
Hypercoagulability - Due to Cancer, sepsis, Genetic conditions, Protein S and C deficiency Surgery, Contraceptive pill
Endothelial damage - Smoking, Diabetes, Hypertension
Venous stasis - Heart failure, DVT Recent surgery, bed bound or long haul flight
taken from https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.113.004586
Other than factors that can lead to a PE through influencing Virchow’s triad, what are some more rare causes that can lead to a PE?
- **Right ventricular thrombus (post-MI)
-
Septic emboli (right-sided endocarditis - bacterial vegetation)
Air Embolus
Parasites
Forgein Materail from IVDU
Fat Emboli
What is a thromboembolism? What can it lead to, regarding alveoli?
A piece of clot that have broken free
Can lead to Thromboembolism - Clog in a tiny artery leading to a decrease in oxygen. Alveoli will receive air but no blood, leading V/Q mismatch
unable to produce surfactant, which leads to alveolar collapse and an increased lack of oxygen in the body (hypoxaemia).
What are some signs of pulmonary embolism?
think RSHF?
-Hypoxia
- Cyanosis may be present
- Deep vein thrombosis: swollen, tender calf
- Pyrexia may be present
- Tachypnoea and tachycardia
- Crackles
- Hypotension: SBP <90 mmHg suggests a massive PE
- Elevated JVP: suggests cor pulmonale
- Right parasternal heave: suggests right ventricular strain
What would be some symptoms of PE?
- Pleuritic chest pain
- Dyspnoea
- Cough +/- haemoptysis
- Fever
- Fatigue
- Syncope: a red flag symptom
taken From https://www.verywellhealth.com/symptoms-of-pulmonary-embolus-4163779
What are some investigations to carry out for a suspected pulmonary embolism patient?
- CXR:performed to rule out alternative pathology. It is typically normal in a PE, although a wedge-shaped opacification may be seen
- ECG:
- CT pulmonary angiogram (CTPA): highlights the pulmonary arteries to demonstrate any blood clots.
- D-dimer:detect fibrin breakdown products
- Other investigations to consider
- ABG:to quantify the degree of hypoxaemia; also respiratory alkalosis if there is hyperventilation that gets rid of CO2
- V/Q scan: involves using radioactive isotopes and a gamma camera to reveal areas of the lung that are ventilated but not perfused. Done in patients allergic to contrast, with severe renal impairment and also considered in pregnancy
- Pulmonary angiography:gold-standardbut more invasive and has higher complications
What are some preventative measures for PE?
- Compression stockings
- Frequent calf exercises during long periods of sitting still
- Prophylactic treatment with low molecular weight heparin
How would you manage someone with a massive PE?
Oxygen if Hypoxic, and morphine if needed
Get IV access with LMWH or Fondaparinux
Give Bolus 500ml IV fluid if hypotensive
Haemodynamically unstable - Thrombolysis, eg alteplase - either IV or directly into pulmonary arteries with central catheter
How would you manage someone with a non massive PE? For someone with a renal impairment and someone without a renal impairment
No renal impairment
§ Offer apixaban or rivaroxaban (Inhibits thrombin)
§ If neither suitable, offer one of:
□ LMWH for at least 5 days followed by dabigatran or
edoxaban (Inhibits thrombin)
Renal impairment (estimated creatinine clearance <15 ml/min)
§ Offer one of:
□ LMWH (Low Molecular Weight Heparin.)
□ Unfractionated heparin (UFH)
What are some complications of a PE?
Heparin treatment = decrease in platelet count, known as hepatic-associated thrombocytopaenia.
Obstruction of pulmonary vasculature= resulting in pulmonary hypertension and subsequent strain on the right heart =Cor Pulmonale.
Pulmonary infarction, tissue necrosis.
Sudden death due to large pulmonary thromboembolism
Hyperventilation in response to the embolism can cause a rapid release of CO2, resulting in respiratory alkalosis.
AVSD - Emboli can travel to brain, and cause an embolic stroke
How many layers does a true aneurysm involve?
How many layers of the arterial wall does a false/pseudo-aneurysm involve?
A true aneurysm is one that affects all three layers of the arterial wall - the endothelial cells of the tunica intima, the smooth muscle of the tunica media, and the connective tissue of the tunica adventitia,
On the other hand, a false/pseudo-aneurysm only involves one layer of the arterial wall, for example, the tunica intima in aortic dissection.
What are the two major types of true aneurysms?
fusiform aneurysms, which are uniform in shape with symmetrical dilatation and involves the entire circumference of the aortic wall;
saccular aneurysms = local outpouchings of only a portion of the aortic wall.
What is an abdominal aortic aneurysm?
An abdominal aortic aneurysm (AAA) describes a dilatation in vessel wall diameter of >50%, which typically means a diameter of >3 cm
What are some risk factors to get an abdominal aortic aneurysm?
- Increasing age
- Male gender
- Atherosclerosis
- Smoking
- Hypertension
- Hyperlipidaemia
- Diabetes
- Connective tissue disorders: such as Ehlers Danlos and Marfan syndrome, due to changes in the balance of collagen and elastic fibres
- Family history
Where are abdominal aortic aneurysms most likely to occur? Why is this?
The abdominal aorta usually develops an aneurysmbelow the renal artery level.
Below renal arteries, the aorta lacks the small blood vessels (vasa vasorum) in its adventitial layer which are necessary to supply the aorta with nutrients.
Therefore, the middle layer of the aorta is prone to ischaemia, making an aneurysm more likely.
Normal physiology - what are the 3 main layers in an artery wall? What is in each of them?
- Tunica Interna (Endothelium): This innermost layer is composed of a single layer of flat, squamous endothelial cells that are supported by a thin basement membrane.
- Tunica Media: This layer is composed of multiple layers of smooth muscle cells, separated by layers of elastic fibers.
- Tunica Adventitia: This outermost layer is composed of connective tissue and collagen fibers that provide structural support for the artery wall.
What is the most common cause of AAA? Outline the pathophysiology behind it
Atherosclerosis
Atherosclorosis - Enzymes released in inflammation lead to breakdown of extracellular matrix found in tunica media, === weakens structure of aortic wall
Also the persistent inflammation weakens the arterial wall
What are other causes aortic aneurysms/ aneurysms in other arteries in the body?
Atheroma – persistent inflammation weakens the arterial wall
Trauma
Connective disorders
Inflammatory AAA - so by smoking, atheroslcorosis, and vasculitis
Maran’s syndrome
Ehlers-Danlos syndrome
Infection
Other causes of AAA:
What is
a) Inflammatory AAA
b) Marfans Syndrome
InflammatoryAAA = usually affectsyounger patientsand is associated with smoking, atherosclerosis and vasculitis, accounting for 5-10% of aortic aneurysms cases. Presents similarly to a normal AAA but may also be associated withfever.
Marfan’s – gene coding for fibrillin-1 affected (fibrillin-1 used in ECM structure)
What are some signs of aortic aneurysms? When would you see these?
In general, aneurysms are not associated with any symptoms and are often found by chance. In contrast, signs and symptoms may be present if the aneurysm has ruptured or is likely to rupture.
- Signs
- Pulsatile abdominal mass
- Tachycardia and hypotension: red flags signifying ruptured AAA
- Grey-Turner’s sign:
- Cullen’s sign:
Signs of Aortic anuerysms - what is
a) Grey-Turner’s Sign
b) Cullen’s Sign?
- Grey-Turner’s sign: flank bruising secondary to retroperitoneal haemorrhage
- Cullen’s sign: pre-umbilical bruising
What are some symptoms of aortic aneurysms?
- Flank, back or abdominal pain
- Pulsating abdominal sensation
Ruptured ones:
Shock, An expansible abdominal mass that rises and contracts
Collapse
intermittent or continuous abdominal pain
What is the main investigations to consider if you suspect an Aortic aneurysm?
Abdominal ultrasound: definitive diagnosis with high sensitivity (92-99%) and specificity (~100%)
What are some other tests you can do for suspected Aortic aneurysm?
- FBC: leaking AAA may cause anaemia, inflammatory AAA may cause leukocytosis
- U&Es: baseline renal function is important prior to a CT angiogram as it requires contrast, whilst hypovolaemia may cause pre-renal acute kidney injury
- CRP/ESR: raised in inflammatory AAA
- Group and save & crossmatch: vital if a ruptured AAA is suspected in order to ensure blood is available for transfusion
- CT angiogram: for more detailed anatomical information, particularly if near the renal arteries; it is also the test of choice for pre-operative planning
- MRI: MRI is preferred over CT for females of child-bearing age and those allergic to iodinated contrast
What screening is offered to all males over 65 for abdominal aneursyms?
The screening programme in England is offered to all males aged 65 and over as a one-off abdominal ultrasound and further surveillance is organised if the aneurysm exceeds 3 cm.
<3 cm - discharge from screening
3 -4.4 cm - Annual Surveillance
4.5-5.4 cm - 3 monthly surveillance
>5.5 cm - Refer to vascular surgeon to be seen within 2 weeks of a diagnosis
Outline some of the types of management there is for abdominal aortic aneurysms.
Treatment
Lifestyle advice, Surveillance, BP control, Statins, controlling cardiovascular co-morbidities
Or
Surgery - eg Endovascular Aortic repair
Antiinflammatorys if its inflammatory aka steroids of immunosuppressants
What is the emergency management for someone with a ruptures AAA?
Summon a vascular surgeon, warn theatre - you have to operate!
Do ECG, take blood for amylase
Catheterise bladder
Gain IV access with 2 large-bore cannulae
Treat shock with ORh-ve blood, but keep BP <100mmHg to avoid rupturing a contained leak
Take patient straight to theatre
Give prophylactic antibiotics, eg co-amoxiclav**
Surgery involves clamping the aorta above the leak, and inserting a tube graft
What is an aortic dissection?
TUNICA INTIMA SPLITS, BLOOD FLOWS INTO FALSE CHANNEL BETWEEN TUNICA INTIMA AND MEDIA – MEDICAL EMERGNCY, CAN LEAD TO RUPUTRE
What are some risk factors for aortic dissection?
- Hypertension: the most important risk factor
- Smoking
- Family history of aortic aneurysm or dissection
- Coarctation of the aorta: narrowing of vessel
- Bicuspid aortic valve
- Connective tissue disorders:Marfan and Ehlers-Danlos syndrome
- Turner and Noonan syndrome
- Trauma
- Pregnancy: increased blood plasma volume
- Syphilis
According to Haroon, obesity is not a risk factor for aortic dissection!!
What happens in aortic dissection?
Where does it most commonly occur?
As the high-pressured blood continues to shear more and more of the tunica intima off the tunica media, blood starts to pool between the two layers, increasing the outside diameter of the blood vessel.
The area where blood collects between intima and media is called a false lumen.
This most commonly occurs around the ascending aorta and aortic arch, but can affect any part of the aorta.
Aortic dissection pathology -
How can a double barrelled aorta form?
What is it called when the dissection tracks back to the pericardium?
Sometimes, the lumen will be taken back into the primary lumen, = forms ‘double-barrelled aorta’ that may be stable yet may also rupture.
Dissections can affect valves, if dissection reaches pericardium, will cause a Hemopericardium
Dissection is a medical emergency and has to be treated asap. If the blood manages to escape through all the layers of the wall of the aorta, then rupture is the result.
Aortic dissection classification - what is the Stanford classification?
Stanford:
- Type A: dissection involves the ascending aorta with or without the involvement of the arch and descending aorta, occurringproximalto the left subclavian artery (⅔ of cases)
- Type B: dissection doesnotinvolve the ascending aorta. Involves only the descending thoracic or the abdominal aorta, occurringdistalto the left subclavian artery (⅓ of cases)
What are some signs of aortic dissection?
- Weak downstream pulses: radio-radial and/or radio-femoral delay - Absent peripheral pulses
- A difference in blood pressure between two arms: >10 mmHg
- Hypertension
- Tachycardia and hypotension: as condition progresses
- Diastolic murmur: due to aortic regurgitation
-
Involvement of specific arteries
- Spinal arteries → paraplegia
- Coronary arteries → angina
- Distal aorta → limb ischaemia
What are some symptoms of aortic dissection?
- Sudden onset, severe ‘tearing’ or ‘ripping’ chest pain that may radiate to the back
- Syncope: red flag symptom
Pain usually follows the line of the dissection
Ascending aorta – pain will be in the chest
Descending aorta – pain often in the back
Collapse (due to hypotension)
Expansile (not pulsatile) mass in the abdomen
Shock
Hypotension
Tachycardia
Profound anaemia
Sudden death
Testicular pain
Symptoms similar to renal colic
Symptoms similar to diverticulitis
Non-specific back pain – this results from gradual erosion of the vertebral bodies in patients with long-standing aneurysm.
What are some investigations for aortic dissection?
CT/MRI angiography confirms diagnosis – contraindicated in patients with renal disease
CXR – shows widened mediastinum/aorta
Transoesophageal echocardiogram
FBC:anaemia may be present
ECG:non-specific changes such as T-wave inversion or ST-segment depression. ST-segment elevation may be seen in the inferior leads in some patients
What is the management of a Type A aortic dissection?
- Blood transfusion
- Beta blocker e.g. IV labetalol: aim for a systolic blood pressure of 100-120 mmHg; high pressures are associated with extension of the dissection
- Urgent surgical repair/ stenting: open surgery with replacement of the ascending aorta should be performed immediately upon diagnosis
Type A - dissection involves ascending aorta, with or without involving the arch/descending aorta. Happens Proximal to the left subclavian artery
What is the management of a Type B aortic dissection?
-Type B
Conservative management - Bed rest
Hardcore beta blocker, eg IV Labetalol - aim for systolic BP 100-120 - monitor closely in high dependency unit
Open surgery, (often still treatment of choice) or Thoracic endovascular aortic repair
Type B - does not involve ascending aorta, only descending **Occurs distal to the left subclavian artery
What are some complications of aortic dissection?
Aortic regurgitation: Dissection of the aorta causes weakening of the support of the leaflets of the valve.
Myocardial infarction: Damage to the aorta that propagates in an upward direction can lead to an ST-elevation on the right side of the heart.
Stroke: A tear in the aorta can interrupt the supply of blood to the brain.
Renal failure: The false lumen created by the dissection can put pressure on the renal arteries, decreasing the flow of blood to the kidneys.
Pericardial tamponade: Blood from the false lumen of the aorta can leak into the pericardial space, leading to a medical emergency known as pericardial tamponade.
Haemorrhage and shock: Disruption of the walls of the aorta due to the dissection can cause the blood to rush out, leading to a rapid loss of blood and shock.
What is peripheral vascular disease?
Peripheral vascular disease (PVD) is a long-term illness brought on by the narrowing of blood vessels in the arms and legs resulting from atherosclerosis.
The severity of the symptoms correlates with the degree of arterial blockage. The cause and risk factors for this condition are the same as for coronary artery disease (CAD).
What are some risk factors for peripheral vascular disease?
Hypertension
Dyslipidaemia
High LDL and low LDL levels
Diabetes
Obesity
FHx of arterial disease
Significant if a first degree relative had MI before the age of 55
Smoking
Age
Male gender
What is a classic presentation for peripheral vascular disease?
Aching in calves - claudication - relieved by taking a break
Pain when legs are elevated, if bed bound - relieved when lowering
Claudication = think angina of the limbs
What things would you do in order to examine for peripheral vascular disease?
Pale and cold leg on elevation - (Beuger’s angle <20’) – the leg will go pale and cold upon raising it 20’ off the couch.
Increased vascular filling time– Upon lowering, the leg may become hot and red as reperfusion occurs.
Perfusion time tends to be increased (>15s)
Oedema is not usually present
Evidence of poor skin health eg ulcers, dry scaly skin, cool peripheries and reduced capillary refill time
Absent (posterior tibial and dorsals pedis) pulses represent an increased chance of peripheral vascular disease
What are some thing you may see as complications of severe Peripheral vascular disease?
‘Punched out’ ischaemic ulcers – usually on the toes and heels, rarely higher up the limb. These tend to occur after a localised traumatic event.
.
Gangrene – often black necrotic gangrenous tissue surrounds the punched out ulcer lesions. Infection of this areas can occur (wet gangrene).
Reduced / absent peripheral pulses – start distally, and work your way up until you find the pulse
Skin atrophy – in chronic disease
Hair loss – in chronic disease
Cyanosis
Excessive sweating – due to overactivity of the sympathetic nerves
Erectile Dysfunction –
Amputation may be necesscary!
What is ABPI? What can it be used for?
Ankle Brachial pressure index - Compares Blood pressure in Arms and legs, as reduced blood flow to legs is more common than arms in PVD.
Used alongside a suggestive examination and history to diagnose PVD
How do you carry out ankle-brachial pressure index? What values suggest
a) Normal
b) lower limb ischaemia
c) Pain at rest
d) high risk of gangrene
Divide systolic ankle pressure by systolic brachial pressure
A normal value is >1
A value of <0.9 is pathological for limb ischaemia (PVD).
lower the number, the greater the degree of PVD
Pain at rest – ABPI = <0.6
High Risk of gangrene – ABPI – <0.3, or ankle systolic pressure <55mmHg
CAUTION – in very severe arteriosclerosis the vessels are incompressible, and thus falsely high readings may be obtained (e.g. an ABPI >1.3)
What is the management for Peripheral vascular disease?
No medications proven to help with claudication
Walking therapies and exercise encouragement!
Statin (Atorvastatin)
Ace Inhibitor - Ramipril
Beta blockers - should be avoided, unless PAD is severe
Antiplatelet agent - Aspirin, clopidogrel
What causes the formation of venous ulcers?
What causes the formation of arterial ulcers?
Arterial ulcers develop as the result of damage to the arteries due to lack of blood flow to tissue. Ischaemia
Venous ulcers develop from damage to the veins caused by an insufficient return of blood back to the heart. (Stagnation of blood under pressure)
Outline some features of arterial ulcers, that are comparable to venous ulcers
Arterial ulcers
Occur distally, affecting the toes or dorsum of the foot/lateral malleolus
Are smaller and deeper than venous ulcers
Well defined borders
Have a “punched-out” appearance
Are pale colour due to poor blood supply
Are less likely to bleed
Are painful
Have pain worse at night (when lying horizontally), and on elevating, and then improved by lowering the leg
Outline some features of venous ulcers, that are comparable to arterial ulcers
Occur in the gaiter area (between the top of the foot and bottom of the calf muscle), and medial malleolus
Are larger and more superficialthan arterial ulcers
Have irregular, gently sloping border
Are more likely to bleed
Are less painful than arterial ulcers
Have pain relieved by elevation and worse on lowering the leg
When would someone need surgery for PVD? What procedures would be done?
Lifestyle limiting claudication
Pain at rest
Gangrene
Percutaneous Transluminal angioplasty – PTA
What is angina?
Angina refers to classic cardiac pain that is felt when there is a reduction in blood supply to the heart.
What are some risk factors for angina?
- Non-modifiable: increasing age, male gender, family history
- Modifiable:hypertension, diabetes, obesity, hypercholesterolaemia, smoking, cocaine use, stress, sedentary lifestyle
What is the pathophysiology behind stable angina?
reduced blood flow which causes ischaemia, leads to chest pain.
It usually occurs when the patient has greater than or equal to 70% stenosis. –> so can supply enough blood at rest to heart, but not enough during exertion
Patient’s experience symptoms during these times of stress but symptoms are relieved with rest.
Outline the formation of an atherosclerotic plaque in a vessel wall.
Damage to arterial walls results in inflammation that promotes the formation of atheromatous plaques.
Monocytes scavenge lipids upon entry into the arterial wall, transforming into foam cells.
Cytokinesare released by foam cells, promoting smooth muscle migrationfrom the arterial media into the intima.
Over time, plaques develop in size.
What other heart conditions can lead to stable angina?
Hypertrophic cardiomyopathy ( needs more O2)
Aortic stenosis
- Valvular disease
- Arrhythmias
- Embolus to the coronary artery
- Vasculitis: causing aneurysm
- Anaemia: less O2 is transported to the heart
What are some signs of Stable angina?
- Xanthomas or xanthelasma: suggests hypercholesterolaemia
-
Hypertension
- A risk factor for angina
- Retinopathy may be seen on fundoscopy
- Evidence of peripheral vascular disease: may coexist with ischaemic heart disease
What are some symptoms of stable angina? How would you differentiate between stable and unstable angina?
If the pain doesn’t resolve within 5 minutes of cessation of activity, and/or with use of GTN spray, treat as ACS
Angina can be precipitated by exertion, heavy meals, cold weather and emotion
- Cardiac-sounding chest pain
- Crushing, left-sided chest pain
- Often radiating to neck, jaw, shoulders and left arm
- Dyspnoea
- Nausea
- Sweating
What investigations would you carry out in suspected stable angina?
Physical examination, ECG
Chest X ray
Exercise tolerance test
CTCA - A type of high resolution CT scan, with contrast – injected through a peripheral cannula A non-invasive test takes about 10-15 seconds. Scan conducted whilst patient holds their breath, the contrast fills the coronary arteries and can indicate where they are narrowed
Cardiac MRI
Stress Echo
What medication can you give to treat stable angina
a) Symptom relief
b) managing long term
Stuff for symptom relief - GTN spray or tablet, a vasodilator
- 1st line: **β-blocker calcium channel blocker, aka verapamil
- 2nd line: dual therapy with dihydropyridine calcium channel blocker AND β-blocker
-
3rd line: add additional anti-anginal medication e.g.
- Nitrates
- Ivabradine
- Nicorandil
- Ranolazine
What are some preventative measures for stable angina?
- Lifestyle changes: exercise, dietary alterations, lipid, diabetes and hypertension management, smoking cessation
- Aspirin and astatin
- Angiotensin-converting enzyme inhibitors(ACEi): if the patient has angina and diabetes
What is Prinzmetal angina? What are some risk factors for it?
Angina due to coronary spasm, which can occur even in normal coronary arteries. Smoking is a risk factor for it, and cocaine/amphetamine use can trigger it.
Hypertensions and hypercholesterolaemia are not risk factors for it!!
What is the treatment for Prinzmetal angina?
Avoid triggers
Correct low magnesium
Stop smoking
Give GTN when needed
Calcium channel blockers and/or long acting nitrates.
What is Rheumatic fever? Outline the pathophysiology that happens in it
Group A beta-haemolytic streptococcus, typically streptococcus pyogenes, can cause tonsillitis which subsequently leads to rheumatic fever.
The body’s immune system produces antibodies to battle the infection, however, these antibodies also mistakenly identify some of the individual’s cells as foreign and attack them, resulting in a type 2 hypersensitivity reaction.
This delayed response usually occurs between 2 and 4 weeks after the onset of the initial infection.
Why is rheumatic fever rare in developed countries?
It is rare in the UK due to early treatment of streptococcus with antibiotics.
What is a typical presentation of Rheumatic fever?
The typical presentation of rheumatic fever occurs 2 – 4 weeks following a streptococcal infection, such as tonsillitis. Symptoms affect multiple systems, causing:
Fever
Joint pain
Rash
Shortness of breath
Chorea
Nodules
Heart involvement, nervous system involvement
What can rheumatic fever do to the heart?
can lead to Carditis, or inflammation throughout the heart, with pericarditis, myocarditis and endocarditis, leads to:
Tachycardia or bradycardia
Murmurs from valvular heart disease, typically mitral valve disease
Pericardial rub on auscultation
Heart failure
What can rheumatic fever do to the skin and nervous system?
Skin Subcutaneous nodules =
Firm painless nodules occur over extensor surfaces of joints, such as the elbows.
Erythema marginatum ==
rash pink rings of varying sizes affecting the torso and proximal limbs
Chorea is the key nervous system symptom. This involves irregular, uncontrolled and rapid movements of the limbs. This is also known as Sydenham chorea and historically as St Vitus’ Dance.
What investigations can you do for rheumatic fever?
Throat swab for bacterial culture
ASO antibody titres
Echocardiogram, ECG and chest xray can assess the heart involvement
A diagnosis of rheumatic fever is made using the Jones criteria (see below).
Anti-streptococcal antibodies (ASO) are antibodies against streptococcus. They indicate a recent streptococcus infection and can be helpful in supporting a diagnosis of rheumatic fever.
What is the management of rheumatic fever?
Patients with clinical features of rheumatic fever should be referred immediately for specialist management. Management involves medications and follow up:
NSAIDs (e.g. ibuprofen) are helpful for treating joint pain
Aspirin and steroids are used to treat carditis
Prophylactic antibiotics (oral or intramuscular penicillin) are used to prevent further streptococcal infections and recurrence of the rheumatic fever. These are continued into adulthood.
Monitoring and management of complications
to prevent rheumatic fever, what should give to treat tonsillitis caused by streptococcus?
Tonsillitis caused by streptococcus should be treated with phenoxymethylpenicillin (penicillin V) for 10 days.
What happens in restrictive cardiomyopathy? How can this lead to heart failure?
Restrictive cardiomyopathy describes when the heart muscle becomes stiffer and less compliant.
However, the muscles and size of the ventricles stay roughly the same size, or only get slightly enlarged
When blood fills restricted ventricles, however, they can’t expand as much. This means the ventricles fill with less blood and therefore pump out less blood. This eventually leads to heart failure
What investigations would you do for restrictive cardiomyopathy?
- ECG: low amplitude QRS
- ECHO
- CXR
- MRI
- Cardiac catheterisation
What are some of the causes of restrictive cardiomyopathy?
Amyloidosis - amyloid deposition in the heart
- Sarcoidosis - Formation of granulomas in the heart
- Haemochomatosis - iron overload = iron in the heart
Scerloderma - chronic connective tissue disease leading to hardening
What is dilated cardiomyopahty?
Dilated cardiomyopathy refers to when all 4 chambers of the heart dilate (but don’t get thicker).
What are some causes of dilated cardiomyopathy?
Most often idiopathic
- Autosomal dominant - familial
- Certain genetic conditions e.g. Duchenne Muscular Dystrophy and haemochromatosis
- Infection e.g. coxsackievirus B or Chagas disease, a protozoal infection
- Alcohol abuse: alcohol and its metabolites have a direct toxic effect on the myocardium
- Chemotherapy drugs e.g. doxorubicin and daunorubicin
- Drugs e.g. cocaine
- Thyroid disorder
- Peripartum cardiomyopathy: dilated cardiomyopathy can develop in the third trimester of pregnancy
What can dilated cardiomyopathy lead to?
Pathophysiology
New sarcomeres added, however walls remain thin
Leads to weak contractions, and a lower stroke volume - leads to Biventricular heart failure
Also, enlarged chambers press on valves, leading to regurgiation/systolic murmur, and stretching of walls can lead to arrhythmias
blood rushing and slamming into the dilated ventricular wall during diastole –> S3 heart sound
What are some clinical signs of dilated cardiomyopathy?
- Larger heart seen on imaging
- Systolic murmur: due to regurgitation
- S3 gallop: due to blood rushing hitting the dilated ventricular wall during diastole
- Increased pulse
- Decreased BP
- Arrhythmias
- Signs of heart failure e.g. pulmonary oedema, increased JVP
What investigations would you do for suspected dilated cardiomyopathy? What would these investigations show?
- Bloods: BNP elevated; low Na+ implies poor prognosis
- CXR: cardiac enlargement; pulmonary oedema
- ECG: tachycardia, non-specific T wave changes and poor R-wave progression; may be AF or VT
- ECHO: shows dilated heart and low ejection fraction
What is the management for dilated cardiomyopathy?
- Bed rest
- Diuretics: to deal with oedema
- Beta blockers: to control heart rate
- ACE inhibitors: dilate vessels to improve blood flow
- Anticoagulation: due to increased risk of thrombus
- Biventricular pacing
- ICD - implantable cardioverter defibrillator
- Left ventricular assist device (LVAD): mechanical pump that assists the heart in distributing blood
- Heart transplant, in extreme cases
What is hypertrophic cardiomyopathy?
Hypertrophic cardiomyopathy (HCM) is a genetic disorder characterised by left ventricular hypertrophy (LVH).
IT IS AUTOSOMMAL DOMINANT CONDITION
It is a primary form of cardiomyopathy i.e. not in response to other underlying disease e.g. hypertension or valvular disease
What is the pathophysiology behind the consequences of hypertrophic cardiomyopathy?
IT IS AUTOSOMMAL DOMINANT CONDITION
- Walls take up more room so the cavity is smaller and less able to fill with blood.
- Walls are more stiff and less compliant so can’t stretch to fill with more blood.
- This means less blood is pumped out of the heart - stroke volume is reduced. This can lead to heart failure.
Muscle growth of IV septum, obstructs blood leaving LV and pulls anterior leaflet of mitral valve down ==> leads to crescendo-descrendo murmur
Bigger heart means more O2 needed ( ==> ischaemia) and more disarray of myocytes (==> Arrhythmias)
What are some signs of hypertrophic cardiomyopathy?
- Ejection systolic murmur: crescendo-decrescendo character due to blood flowing through the obstructed left ventricular outflow tract.
- Bifid pulse: two pulses due to mitral valve moving towards outflow tract mid-systole and causing further obstruction
- S4 sound: due to atria contracting and pushing blood into a non-compliant ventricular wall during diastole.
- Systolic thrill may be felt
- Arrhythmias
- Hypertrophy seen on imaging
What investigations would you do for suspected hypertrophic cardiomyopathy? What would they show
Left axis deviation.
- ECG: progressive T wave inversion and deep Q waves; may also be AF, WPW syndrome, ventricular ectopics, left axis deviation
- Echocardiogram: shows ventricular hypertrophy and a small left ventricular cavity; mid-systolic closure of aortic valve; anterior movement of mitral valve mid-systole
-
MRI
Exercise test
Genetic analysis can confirm diagnosis since most cases are autosomal dominant and familial
What are some of the treatment options for hypertrophic cardiomyopathy?
Beta blockers or calcium channel blockers: control heart rate. (Don’t give digoxin as can increase force of contraction which can worsen condition)
- Anti-arrhythmic medication e.g. amiodarone
- Consider defibrillator if at high risk of arrhythmias
- Anticoagulation: if AF is present as there is higher risk of thrombus formation
- Septal myectomy: surgery to remove part of septum causing obstruction
There’s been a lot of talk about calcium channel blockers, but how exactly do they work?
Calcium channel blockers are medications used to lower blood pressure.
They work by preventing calcium from entering the cells of the heart and arteries. Calcium causes the heart and arteries to squeeze (contract) more strongly. By blocking calcium, calcium channel blockers allow blood vessels to relax and open.
What are the four things that characterise tetralogy of Fallot?
Pulmonary stenosis
Right Ventricular hypertrophy
Ventricular septal defect
Overriding aorta
It is the most common form of congenital cyanotic heart disease
Pathophysiology of tetralogy of Fallot - what does
a) Pulmonary stenosis
b) Ventricular septal defect
c) Overriding aorta
all lead to/cause?
TETROLOGY OF FALLOT -
Pulmonary stenosis - leads to RV hypertrophy as it has to push harder to get blood through
VSD - blood shunts from right to left due to RV hypertrophy - Deoxygenated blood enters circulation
Overriding Aorta - Entrance to aorta is further right then normal, above VSD - so more deoxygenated blood enters aorta when the RV contracts upwards
Would a baby born with tetralogy of fallot be cyanotic? Why?
YES! There is a greater pressure in the RV than the LV and so blood is shunted into the LV -> CYANOSIS!
What are some risk factors for tetralogy of fallot?
- Neonates and babies: typically manifests at around 1-2 months of life
- Family history of congenital heart disease
- Rubellainfection
- Increased age of the mother (over 40 years)
- Alcohol consumption in pregnancy
- Diabetic mother
- Down syndrome: trisomy 21
What are soem clinical manifestations of tetralogy of fallot?
- Signs
- Ejection systolic murmur: due to pulmonary stenosis
- Reduced SpO2, particularly when distressed
- Respiratory distress
- Cyanosis
- Clubbing
- Symptoms
- Poor weight gain or ‘failure to thrive’
- Difficulty feeding
- Hypercyanotic or ‘tet’ spells: cyanosis, breathlessness and syncope, particularly when crying or feeding
- Squatting posture
What would an ECG and Echocardiogram of a patient with tetralogy of fallot show?
- ECG:evidence of right ventricular hypertrophy, such as right axis deviation
- Echocardiogram + doppler flow studies:definitiveinvestigation and will reveal right ventricular outflow obstruction, right ventricular hypertrophy, a ventricular septal defect and an overriding aorta
WILL ALSO SEE A “BOOT SHAPED” HEART
Define coarctation of the aorta. What eponymous syndrome increases the risk of this?
Coarctation of the aorta is defined as a narrowing in the aorta. There is an infant (70%) and an adult form (30%).
Turner’s Syndrome is a risk factor for this
Describe the pathophysiology behind coarctation of the aorta
Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing.
So narrowing of aorta is often just before or after the ductus arteriosus
What can coarcction of the aorta lead to?
In severe cases:
Complete or almost complete obstruction of aortic flow
Patient collapses with heart failure
In moderate Cases;
Raised BP
Systolic murmur from collateral vessels – best heard over left scapula (scapula bruit)
What are some long term problems that can be caused by coarction of the aorta?
Hypertension
Early coronary artery disease
Early strokes
Sub arachnoid haemorrhage
Re-coarctation requiring repeat intervention
Aneurysm formation at the site of repair
teenager with high blood pressure - think coarction of the aorta
What are some signs and symptoms of coarctation of the aorta?
Signs and Symptoms:
Often asymptomatic for many years
Right arm hypertension
Radio-femoral pulse delay – will feel radial pulse BEFORE femoral pulse
Discrepant BP in upper and lower body
Bruits (buzzes) over the scapulae and back from collateral vessels
Mid systolic murmur
teenager with high blood pressure - think coarction of the aorta
Headaches and nose bleeds (due to hypertension)
What is the management of coraction of the aorta?
What can be a complication of management?
Management
Surgical repair
Percutaneous repair
Balloon dilation (preferred for re-coarctation) and stenting
RISK OF ANEURYSM FORMATION AT SITE OF REPAIR
What is the most common congenital heart defect? Outline what it is.
Ventricular Septal Defect
When the ventricular septum has a gap in it.
This can vary in size from tiny to the entire septum, forming one large ventricle.
Outline the pathophysiology behind Ventricular septal defect, initally
Oxygenated blood then enters the left atrium and then the left ventricle. Here, blood travels from the high pressure LV to the low pressure RV (left to right shunt). The blood flowing through the VSD causes a holosystolic murmur
At this point, patient’s are acyanotic as there is no deoxygenated blood entering the systemic circulation.
What can happen overtime in a patient with VSD? What condition can they go on to develop?
Overtime, this causes increase of blood in Right sided circulation = causing an increase in pressure.
Now shunt is reversed = deoxygenated blood enters the systemic circulation via the aorta and cause cyanosis - this is known as Eisenmenger syndrome.
What are some signs and symptoms of VSD?
- Signs
- Pansystolic murmur at the lower left sternal border
- May be a systolic thrill on palpation
- Cyanosis: due to deoxygenated blood in systemic circulation
- Tachypnoea
- Symptoms
- Dyspnoea
- Poor feeding
- Failure to thrive
What is the management of VSD?
- Watch and wait: for small VSD as they can close spontaneously
-
Surgical closure of VSD
- Trans-catheter closure
- Open heart surgery
- Antibiotic prophylaxis: should be considered due to increased risk of infective endocarditis
What is the most common congenital heart defect seen in adults? define what it is.
Atrial septal defect - opening in the heart between the right and left atria.
What are the clinical manifestations of ASD?
Significant increase in blood flow through the right heart and lungs - pulmonary flow murmur.
Enlarged pulmonary arteries.
Right heart dilatation.
SOBOE.
Increased chest infection.
- Mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border
- Splitting S2 sound: due to pulmonary valve closing after the aortic valve
What is the management for someone with ASD?
- Watch and wait: for small ASD as it may spontaneously resolve
-
Surgical closure of ASD
- Trans-catheter closure
- Open heart surgery
- Anticoagulants: used to reduce the risk of clots and stroke in adults
Outline what patent ductus arteriosus is.
Patent ductus arteriosus (PDA) describes the persistent opening of the ductus arteriosus, after birth
Normal physiology - In foetal life, pulmonary vascular resistance is high. Why is this, and what does this lead to?
In a foetus, Bronchioles are filled with Fluid, and pulmonary vessels are constricted due to lack of O2 (Foetus gets O2 from placenta, not lungs)
Pulmonary Vasoconstriction means pressure on right heart is greater than pressure on left heart, ergo flow is from RA => LA via foramen ovale and Pulmonary artery => Aorta via Ducuts arteriosis
Normal physiology - what causes the ductus arteriosis to close in healthy babies at birth? If it remains open, what will it lead to?
At birth, there is an **increased oxygen tension in the blood, and a reduced level of prostaglandins; both of which allow the patent ductus arteriosus to close.
If it remains open then there is an abnormal left to right shunt (aorta to pulmonary artery) and eventually means the lung circulation is overloaded with pulmonary hypertension (leading to Eisenmenger’s syndrome) and right sided cardiac failure (due to RV hypertrophy in response to increased afterload)
What are the main causes of patent ductus arteriosus?
premature babies and cases of maternal rubella
What are some signs at symptoms of patient ductus arteriosus?
Continuous “machinery” murmur
If large, big heart, breathless
Eisenmenger’s syndrome
Differential cyanosis (clubbed and blue toes, but pink not clubbed fingers)
Large:
Torrential flow from the aorta to the pulmonary arteries in infancy
Breathless, poor feeding, failure to thrive
Small:
Little flow from the aorta to Pulmonary arteries
Usually asymptomatic
Murmur found incidentally
Endocarditis risk
What is the management of patent ductus ateriosus?
- Monitor with ECHO until 1 years of age: may close spontaneously
- Indomethacin: NSAID that inhibits prostaglandin E2 so PDA can close
- Trans-catheter closure of PDA
- Surgical ligation of PDA
Define shock.
Type of widespread sudden failure of circulatory system , ==> lack of oxygen reaching bodies cells
leading to insufficient blood flow to the tissues, resulting in cellular damage and harm to multiple organs
If left untreated, can lead to multi organ failure
What are the key clinical manifestations that can define shock?
Often defined by low BP (mean arterial pressure <65mmHg), evidence of tissue hypoperfusion, raised serum lactate.
What 5 main types of shock?
Septic
Anaphylactic –
Neurogenic
Hypovolaemic –
Cardiogenic shock
Sheffield’s, annoying, naughty children’s hospital
define hypovolaemic shock. What are the two types of it?
Hypovolaemic - loss of >20% of body’s fluid/fluid supply, so body cant sufficiently pump enough blood around the body.
Either HAEMORRHAGIC, OR NON HAEMORRHAGIC (due to fluid loss)
Outline some causes of haemorrhagic hypovolaemic shock
Trauma
GI bleeding
Fractures
Ruptured aortic aneurysms
Outline what cardiogenic shock is. What are some causes of it?
Cardiogenic (pump failure) – heart isn’t pumping
Cardiac tamponade.
Pulmonary embolism.
Acute MI.
Fluid overload.
Outline what neurogenic shock is. What typically causes it?
Neurogenic – nervous system damaged so can’t control BP
Classically see hypotension (secondary to massive vasodilation from loss of sympathetic tone), bradycardia and a flushed appearance (again secondary to vasodilation).
Typically caused by a spinal cord injury above T6
Define sepsis.
Sepsis is a condition where the body launches a large immune response to an infection that causes systemic inflammation and affects the functioning of the organs of the body.
Define septic shock
Septic shock is defined when arterial blood pressure drops and results in organ hypo-perfusion
Outline the pathophysiology behind an episode of sepsis - from point of infection to the ensuing oedema (1)
Endotoxins (most commonly found on Gram negative bacteria) get recognised by Macrophages, lymphocytes, mast cells etc and releases various Cytokines, TNF, interleukins, that activate other parts of the immune system, leading to the further release of nitrous oxide and other vasodilators
This causes endothelium of blood vessels to become more permeable, leading to oedema, and decreased intravascular volume
Outline the pathophysiology behind an episode of sepsis - What is the result of oedema and what else happens to reduce oxygen perfusion to organs? (2)
The oedema around the blood vessels decreases the amount of oxygen that reaches the tissues.
In addition coagulation system starts depositing fibrin throughout circulation, which also decreases the perfusion of O2 to organs
Outline the pathophysiology behind an episode of sepsis -What does the deposition of fibrin and excessive consumption of platelets lead to (3)
It also leads to consumption of platelets and clotting factors as they are being used up to form the clots within the circulatory system. This leads to thrombocytopenia, haemorrhages and an inability to form clots and stop bleeding. This is called disseminated intravascular coagulopathy (DIC).
Outline the pathophysiology behind an episode of sepsis - as a result of hypoperfusion, levels of what arise in the blood? (4)
Blood lactate rises due to hypoperfusion of tissues that starves the tissues of oxygen causing them to switch to anaerobic respiration. A waste product of anaerobic respiration is lactate.
What are some risk factors for developing sepsis?
Any condition that impacts the immune system or makes the patient more frail or prone to infection is a risk factor for developing sepsis:
Very young or old patients (under 1 or over 75 years)
Chronic conditions such as COPD and diabetes
Chemotherapy, immunosuppressants or steroids
Surgery or recent trauma or burns
Pregnancy or peripartum
Indwelling medical devices such as catheters or central lines
What signs can you pick up from examination that would be indicitive of sepsis?
High Temp
High Resp rate
O2 sats decreased
Low BP, despite fluids
Reduced urine output
cyanosis
Rigors
Elderly patients often present with confusion or drowsiness or simply “off legs”
Neutropenic or immunosuppressed patients may have normal observations and temperature despite being life threatening unwell
What investigations would you do for suspected sepsis?
Arrange blood tests for patients with suspected sepsis:
Full blood count to assess cell count including white cells and neutrophils
U&Es to assess kidney function and for acute kidney injury
LFTs to assess liver function and for possible source of infection
CRP to assess inflammation
Clotting to assess for disseminated intravascular coagulopathy (DIC)
Blood cultures to assess for bacteraemia
Blood gas to assess lactate, pH and glucose
Additional investigations can be helpful in locating the source of the infection:
Urine dipstick and culture
Chest xray
CT scan if intra-abdominal infection or abscess is suspected
Lumbar puncture for meningitis or encephalitis
Management of sepsis - what is the sepsis 6?
Patients should be assessed and treatment initiated within 1 hour of presenting with suspected sepsis. This involves performing the sepsis six. This involves three tests and three treatments.
BUFALO
Blood Culture
Urine - measure output -
Fluids - get some in
Antibiotics
Lactate - measure
Oxygen - give
measuring urine output will indicate how well the kidneys are perfused - which can indicate perfusion for the rest of the body
What is INR? What is it used for
An INR (international normalized ratio) is a type of calculation based on PT test results.
A prothrombin time (PT) test measures how long it takes for a clot to form in a blood sample.
A PT/INR test is most often used to:
See how well warfarin is working.
Find out the reason for abnormal blood clots
Find out the reason for unusual bleeding
Check clotting function before surgery
Check for liver problems
What is a the target INR for patients taking warfarin?
What happens if INR is too low, and what about too high?
The INR goal for people who take warfarin is usually from 2 to 3.5.
INR levels that are too low may mean you are at risk for dangerous blood clots.
INR levels that are too high may mean you are at risk for dangerous bleeding.
Outline what
Primary
Secondary
Tertiary
prevention all is
Primary prevention prevents the condition developing altogether (eg no smoking, eliminate risk factors before the condn develops)
Secondary prevention aims to tackle a disease that is diagnosed but has not become complicated yet (i.e to manage the disease conservatively before symptoms ensue)
Tertiary prevention is essentially preventing complications of the condition eg surgical procedures, medications
