Cardio Flashcards
(304 cards)
1
Q
Define atherosclerosis
A
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.
2
Q
Outline the progression of atherosclerosis.
A
- 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
3
Q
Fully formed atherosclerotic plaques, can rupture -why is this?
What would a rupture plaque lead to?
A
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
4
Q
What are some risk factors for atherosclerosis?
What is the most significant risk factor for atherosclerosis?
A
age, gender, genetics, smoking, high blood pressure, high cholesterol, diabetes, and obesity.
Hypercholesterolemia is most significant RF for atherosclerosis
development
5
Q
Atherosclerosis - when the endothelium is damaged, what happens that leads to inflammation?
A
the accumulation of LDL-cholesterol in the artery wall, which leads to the activation of inflammatory cells
6
Q
Atherosclerosis - Once the endothelium wall is inflamed, what will begin to accumulate? What does this lead to?
A
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.
7
Q
How does Aspirin help reduce cardiovascular disease? What type of drug is it?
A
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
8
Q
What type of Drugs are
a) Clopidogrel and
b) GPIIba antagonists? What is their effect on the CV system?
A
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
9
Q
What is the main cause of unstable angina, NSTEMI, and STEMI?
What are some other causes of these?
A
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
10
Q
What is the pathophysiology behind the main cause of ACS?
A
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
11
Q
What are some key symptoms of MIs?
A
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!!
12
Q
What is a Silent MI? What % of patients present with it, and it what populations is it most common?
A
MI without chest pain
30% of case of MI present without chest pain.
This is particularly important in:
* Women
* Those with diabetes
* The elderly
13
Q
What investigations would you order for ACS/Suspected MI?
What would you look for on examination
A
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
14
Q
What are the ranges of troponin that are normal, and that could be indicative of an MI?
A
Troponin values <14ng/l normal = no MI, 14-30 ng/l = possible MI, >30ng/l = definite MI
15
Q
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
A
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
16
Q
What are other causes of Raised troponin other than MIs?
A
Causes include:
Renal failure
Myocarditis
PE
Pericarditis
Heart failure
Arrhythmia
17
Q
What ECG changes would you see in a STEMI, immediately??
A
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
18
Q
What ECG changes would you see in a STEMI,
a) within 24 hours
b) within days
A
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
19
Q
What is the first line acute management of ACS?
A
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
20
Q
What are nitrates, like GTN? Why are they given in ACS, and when would you not give them?
A
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 -
21
Q
Once diagnosis of STEMI is confirmed, what is the definitive management?
A
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
22
Q
What do you do with your patient with suspected ACS/NSTEMI, who is unstable?
What is not considered in NSTEMI?
A
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
23
Q
What is thrombolysis? When would you use it in ACS?
A
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
24
Q
How can you assess whether an NSTEMI patient would qualify for a PCI?
A Key part of management!!!
A
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
25
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’)**
26
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
27
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
28
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.
29
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**.
30
In which group is pericarditis most common
When is it 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
31
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)
32
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)*
33
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
34
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**
35
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*
36
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
37
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
38
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)
39
What investigations would you order for suspected pericardial effusion?
CXR – large heart
ECG – low voltage QRS complexes and sinus tachycardia
Echocardiogram
40
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**
41
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*
42
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
43
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*
44
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***
45
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
46
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!!**
47
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.**
48
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
49
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)*
50
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**
51
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
52
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**
53
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.**
54
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)*
55
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*
56
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*
57
What is systolic heart failiure?
What are it's main causes?
Ejection fraction <40% (SV/EDV)
Caused by
IHD
MI
Hypertension
Cardiomyopathy
58
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
59
Name some types of cardiomyopathy
Hypertrophic cardiomyopathy *(can be caused by hypertension, see card on it)*
Dilated cardiomyopathy
Arrhythmogenic Cardiomyopathy
Restrictive cardiomyopathy
60
Outline the pathophysiology of dilated cardiomyopathy
What does it lead to?
Walls either normal or thin 🡪 weak contraction 🡪 less pumped out 🡪 biventricular congestive HF
61
Outline the pathophysiology of arrhythmogenic cardiomyopathy
**Desmosome gene mutations** Lead to arrhyhmias
Arrhythmogenic cardiomyopathy (ARVC/ALVC) –
Arrhythmia main feature of arrhythmogenic cardiomyopathy
62
Outline the pathophysiology of restrictive cardiomyopathy
Restrictive physiology – ventricles stiffer and less compliant 🡪 less CO 🡪 HF
63
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.
64
What are some causes of Right sided heart failure?
Hypertension
Pulmonary stenosis
Lung disease (cor pulmonale)
Atrial/ventricular septal defects
65
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
66
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
67
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)
68
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
69
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
70
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
71
name some investigations for suspected heart failure
ECG
Chest X ray
BNP B-type Natriuretic Peptide levels
Echocardiogram
72
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
73
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**
74
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)*
75
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
76
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*
77
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*
78
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
79
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**
80
Outline some of the key epidemology of aortic valve disease
Most common valve disease
Presenting Patients are normally in their 70s or over
81
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
82
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
83
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**
84
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
85
Where/when is mitral valve stenosis most common?
More common in females, 40-50 years old
86
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
87
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**
88
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
89
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
90
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
91
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)
92
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*
93
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*
94
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
95
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)**
96
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**
97
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.
98
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
99
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.
100
What are the specific breath related symptoms that you see in heart failure (exam fodder)
paroxysmal nocturnal dyspnoea
orthopnoea
Exertional dyspnoea
101
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
102
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**
103
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
104
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*
105
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
106
What does aortic regurgitation lead to?
It leads to a combined volume and pressure overload in the left ventricles
107
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*
108
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
109
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
110
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
111
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
112
What are some risk factors for mitral valve disease?
Risk Factors
* Female
* Lower BMI
* Advanced age
* Renal dysfunction
* Previous MI
113
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**
114
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*
115
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
116
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*
117
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*
118
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
119
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
120
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*
121
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
122
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)
123
Hypertension medication - what is the first line treatment for someone who is black, or over 55 years
calcium channel blocker e.g. amlodipine
124
Hypertension medication - what is the second line treatment for hypertension?
ACE-inhibitor + CCB
Or if afro Caribbean - CCB and ARB
125
Hypertension medication - what is the third line treatment for hypertension?
○ Third line = ACE-inhibitor + CCB + diuretics e.g. Bendroflumethiazide or furosemide
126
Hypertension medication - what is the fourth line treatment for treatment of hypertension?
Fourth line – ACE-inhibitor + beta blocker *e.g. Bisoprolol* + CCB + diuretics
127
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.
128
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**
129
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
130
What are some signs and symptoms 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
* Red, swollen leg (particularly calf)
* Tenderness
* Pitting oedema
* Fever
131
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**
132
What kind of things are included in a Wells score for DVT?
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**
133
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**
134
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
135
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)*
No evidence of use of DOAC if at extremes of weight (less than 40kg or more than 120kg)
Renal impairment (estimated creatinine clearance <15 ml/min)
§ Offer one of:
□ LMWH *(Low Molecular Weight Heparin.)*
□ Unfractionated heparin (UFH)
136
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
137
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
138
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).
139
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
140
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*
141
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-standard** but more invasive and has higher complications
142
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
143
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)
144
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.
145
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
146
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**
147
Where are abdominal aortic aneurysms most likely to occur? Why is this?
The abdominal aorta usually develops an aneurysm**below 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.
148
What is the most common cause of AAA? Outline the pathophysiology behind it
Other causes?
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
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
149
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:**
150
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
151
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**
152
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%)
153
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
154
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
155
Other causes of AAA:
What is
a) Inflammatory AAA
b) Marfans Syndrome
Inflammatory AAA = usually affects younger patients and 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 with fever.
Marfan’s – gene coding for fibrillin-1 affected (fibrillin-1 used in ECM structure)
156
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
157
What is an aortic dissection?
TUNICA INTIMA SPLITS, BLOOD FLOWS INTO FALSE CHANNEL BETWEEN TUNICA INTIMA AND MEDIA -- **MEDICAL EMERGNCY, CAN LEAD TO RUPUTRE**
158
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!!
159
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.
160
What are some signs and symptoms 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
- **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
161
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***
162
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*
163
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**
164
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
165
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**
166
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)*
167
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
168
When would someone need surgery for PVD? What procedures would be done?
Lifestyle limiting claudication
Pain at rest
Gangrene
Percutaneous Transluminal angioplasty – PTA
169
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**
170
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
171
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!!**
172
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.
173
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.
174
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
175
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.
176
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.*
177
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
178
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.
179
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
180
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
181
What is dilated cardiomyopahty?
Dilated cardiomyopathy refers to when all 4 chambers of the heart dilate (but don't get thicker).
182
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
183
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**
184
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
185
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
186
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*
187
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**
188
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
189
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*
190
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!
191
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**
- **Rubella infection**
- **Increased age of the mother** (over 40 years)
- **Alcohol consumption in pregnancy**
- **Diabetic mother**
- **Down syndrome**: trisomy 21
192
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**
193
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:** definitive investigation 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**
194
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
195
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)
196
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)
197
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**.
198
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**
199
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
200
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)
201
What are the main causes of patent ductus arteriosus?
premature babies and cases of maternal rubella
202
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
203
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**
204
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**
205
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.
206
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)
207
What 5 main types of shock?
Septic
Anaphylactic –
Neurogenic
Hypovolaemic –
Cardiogenic shock
*Sheffield's, annoying, naughty children's hospital*
208
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.
209
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
210
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.
211
Define septic shock
Septic shock is defined when arterial blood pressure drops and results in organ hypo-perfusion
212
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
213
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*
214
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***
215
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
216
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*
217
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**
218
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.
219
What is the first line medication given to anyone with T2DM, regardless of age or race?
ACEi, eg Ramipril
220
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 .
221
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)**
222
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
223
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 superficial**than 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
224
What is the intrinsic rate of
a) SA node
b) AV node
c) Ventricular Cells
a) 60-100 beats per minute, the dominate pacemaker
b) 40 - 60 beats a minute
c) 20 -45 beats a minute
*AV node and Ventricular cells are both backup pacemakers*
225
What does a postive deflection show?
Depolarisation waves moving towards an electrode
226
What does negative downwards deflection show?
Depolarisation waves moving away from an electrode
227
Where do the augmented bipolar leads:
Where is the reference (negative) and exploratory (positive) for the
aVR, aVL, aVF leads?
In other words, where do they go from and to?
aVF lead - looks at the flow of charge going from the **The computed average charge of arm electrodes to the left leg**
avR lead - looks at the flow of charge going from the **The computed average charge from the left arm and left leg going to the right arm**
avL lead - looks at the flow of charge going from the **The computed average charge from the right arm and left leg going to the left arm**
Again, always negative to positive! See picutre
228
What ECG leads look at the lateral side of the heart?
Lead I,
Lead aVL
V5 and V6
Lateral = THEREFORE LOOKING AT THE CIRCUMFLEX ARTERY
229
What ECG leads look at the anterior side of the heart?
Therefore what vessel is predominantly looking at?
Leads V3 and V4
DRAW IT OUT
Therefore looking at right coronary artery
230
What ECG leads look at the Inferior side of the heart?
Leads II,
Leads III and
aVF lead
231
Which ECG leads look at the Septum of the heart?
What coronary artery would this be looking at?
leads V1 and V2
AKA LAD artery
232
ECG basic Rules - How long should a healthy PR interval last?
3 - 5 little squares - 0.12-0.2 seconconnds
233
ECG basic Rules - how long should a healthy QRS complex last?
Where does a QRS complex go from and to
No more than 3 little squares
It is from Q-S
234
ECG basic Rules - It what leads should the QRS complex be predominantly upright in?
Lead I and Lead II
235
ECG basic Rules - In what lead are all waves negative in?
Lead aVR
236
ECG basic Rules -In which leads should the T wave **Must** be upright?
Leads I, Leads II and Leads V2 - V6
237
What is the appearance of the P wave in Left atrial enlargement?
What leads would this be best seen?
**Notched/Bifid** P waves,
**Like M, for Mitral, left atria**
Best seen in Limb leads
238
What is the appearance of the P wave in right atrial enlargement?
What leads would this be best seen?
**Tall**, **P**ointed P waves, greater tahn 2.5mm
*Think Right Atria - P for Pulmonale, P for pointed*
239
Exceeding what parameters would deem a Q wave to be pathological?
Greater than 2mm **(Two small boxes deep)**
as well as being greater than one small (1mm) box wide/ greater than 40milliseconds/0.04 seconds
or, **Greater than 25% of the amplitude of the subsequent big R wave**
240
What is represented by
a) one small box
b) one large box
In terms of length and time?
Each (small) horizontal box corresponds to **0.04 sec (40 ms)** and has a **length of 1 mm**
Heavier lines forming larger boxes (thatinclude five small boxes) hence represent **0.20 sec (200 ms) intervals** and are therefore **5mm or 0.5 in length**
241
What are some Pathological common causes of tachycardia?
Atrial fibrillation, Atrial Flutter
Supraventricular tachycardia
Focal atrial tachycardia
Ventricular tachycardia
Ventricular fibrillation
242
What are some common causes of bradycardia?
Conduction tissue fibrosis
Ischaemia
Inflammation/infiltrative disease
Drugs
AV conduction problems
243
Define what a Supraventricular Tachycardia is. What are the 4 types? What is the most common?
Any tachycardia which arises from the atrium or AV junction
Atrial fibrillation
Atrial flutter
AV nodal re-entry tachycardia (AVNRT) **MOST COMMON**
AV reciprocating tachycardia (AVRT)
244
Supraventricular Tachycardias - What is atrial flutter? What things characterise it?
**It is irregular ORGANSIED atrial firing,** around 250 - 300BPM *(conduction pathway typically from around opening of tricuspid valve*
Often associated with AF
Atrial HR = 300 BPM
Ventricular rate = 150/100/75 BPM (due to AV node conducting every 2nd/3rd/4th beat “flutter beat” , *so see at least 2 P waves for every QRS complex* - *but QRS complexes will be regular*
ECG - see flutter waves, which are a saw-tooth pattern of atrial activation, most prominent in leads II, III, aVF, and V1
245
Supraventricular Tachycardias - Name some causes of atrial flutter
- Idiopathic (30%)
- Coronary heart disease
- Thyrotoxicosis
- COPD
- Pericarditis
- Acute excess alcohol intoxication
246
Supraventricular Tachycardias - what would you see on an ECG that would indicate Atrial flutter?
ECG: regular sawtooth-like atrial flutter waves (F waves) with P-wave after P-wave
247
Supraventricular Tachycardias - what is the management of atrial flutter?
- **Treat the reversible underlying condition** (e.g. hypertension or thyrotoxicosis)
- **Rate/rhythm control** with beta blockers or cardioversion (*use of electric shock to put heart back into rhythm)
- **Radiofrequency ablation** of the re-entrant rhythm (*Uses heat generated by radio waves to destroy tissue*)
- **Anticoagulation** based on CHA2DS2VASc score
248
Supraventricular Tachycardias - What characterises AV nodal re-entry tachycardia (AVNRT)?
Most common type of SVT - AV nodal re-entry tachycardia (AVNRT)
Twice as common in women than men
The electrical conduction of the atrium re enters **back through the AV node**, Due to the presence of a “ring” of conducting pathways in the AV node, of which the “limbs” have different conduction times and refractory periods
This allows a re-entry circuit and an impulse to produce a circus movement tachycardia
249
Supraventricular Tachycardias - what is the are the key presentations of someone with AV nodal re-entry tachycardia/AV reciprocating Tachycardia?
***(What's the slightly rogue one)***
Presentation
Regular rapid palpitations – abrupt onset and sudden termination
Neck pulsation – JV pulsations
**Polyuria – due to release of ANP in response to increased atrial pressure during tachycardia**
Chest pain and SOB
Symptoms
Palpitations
Dizziness
Dyspnoea
Central chest pain
Syncope
250
Supraventricular Tachycardias - What is AV reciprocating tachycardia? What is the best known type of this?
The eletrcial signals goes back in the atria via an accessory pathway.
The best known type of this is Wolff-Parkinson-White Syndrome, there is an accessory pathway **(bundle of kent)** between atria and ventricles
251
Supraventricular Tachycardias - What would you see on an ECG of someone with AV Nodal re-entry tachycardia?
P waves are either not visible, or are seen immediately before or after the QRS complex ***(short PR interval)***
QRS complex is a normal shape because the ventricles are activated in the normal way (down bundle of His)
252
Supraventricular Tachycardias - what would you see on an ECG for AV Nodal Reciprocating Tachycardia? (WPW syndrome)
The early depolarisation of part of the ventricle leads:
- shortened PR interval
- **slurred start to the QRS (delta wave)**
- QRS is narrow
Patients are also prone to atrial and occasionally ventricular fibrillation
253
Supraventricular Tachycardias - What is the initial management of AV Nodal re-entry tachycardia and AV Reciprocating tachycardia?
Breath-holding
Carotid massage - *massage the carotid on one side gently with two fingers.*
Valsalva manoeuvre - *Pt blows hard into resistance*
254
Supraventricular Tachycardias - if carotid massage and Valsalva manoeuvre are unsuccessful, what can you give to treat AVNRT and AVRT?
If manoeuvres unsuccessful, **IV adenosine**
Causes a complete heart block for a fraction of a second
Effective at terminating AVNRT and AVRT
255
Supraventricular Tachycardias - What is Atrial fibrilation?
Atrial fibrillation is where the contraction of the atria is **uncoordinated, rapid and irregular.** This is due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node.
This disorganised electrical activity in the atria also leads to **irregular** conduction of electrical impulses to the ventricles.
256
What are some common causes of atrial fibrillation?
PE/COPD
IHD, Heart failure
Rheumatic heart disease, Valve abnormalities
Alcohol intake
**Thyroid issues - Hyperthyroidism**
Sleep Apnoea
Electrolyte disturbances - Hyper/Hypo Kalaemia, Hypo magnesia
PIRATE
257
What are some signs and symptoms of AF?
- **Irregular irregular pulse**
- **Hypotension:** red flag; suggest haemodynamic instability
- **Evidence of heart failure:** red flag; such as pulmonary oedema
- **Palpitations**
- **Dyspnoea**
- **Chest pain:** red flag
- **Syncope:** red flag
Can also be asymptomatic!
258
What investigations would you carry out for AF
ECG
Tests to look for causes of AF:
Serum Electrolytes
Thyroid Function Tests
Cardiac biomarker - eg Troponin
Chest x-ray *look for heart failure*
Transthorasic Echo - *look for functional heart disease*
259
What is the management for someone who is haemodynamically unstable with AF? What signs could indicate that this is the case?
Emergency electrical synchronised DC cardioversion
- **Shock**: hypotension (systolic blood pressure <90 mm Hg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
- **Syncope**
- **Myocardial ischaemia**
- **Heart failure**:
260
What is the first line management for someone who is haemodynamically stable with AF? What signs could indicate that this is the case? What Rate control would you do?
Start by controlling either **rate of rhythm**
Rate control:
- **First line: beta-blocker** (e.g. bisoprolol) or a **rate-limiting calcium-channel blocker** (e.g. verapamil)
- **Digoxin**: may be considered first-line in patients with AF and heart failure
***OF HAEMODYNAICALLY STABLE, DO RATE CONTROL BEFORE RHYTHM CONTROL***
261
What Further management might be necessary for persistent AF/ or AF that has not been treated with meds
Left atrial ablation - small burns/freezes to scar heart tissue to break up electrical signals that cause irregular heartbeats
Electrical DC cardioversion
Anticoagulants - **DOACS** - Apixaban to reduce risk of strokes, or Warafarin if DOACs are CI, (aka in Metal heart valves)
262
Anticoagulants are often given to patient with AF to reduced their likelihood of developing clots that can cause strokes.
What scoring system is used to calculate stroke risk in AF? What types of factors are included on it?
**CHADS2VASc** score used to calculate stroke risk in AF
0 = no anticoagulation
1 = consider oral anticoagulation or aspirin
2 = Anticoagulants - **DOACS** - Apixaban to reduce risk of strokes
Congestive Heart failure = 1
Hypertension = 1
Age > 75 = 2
Age 65-74 = 1
Diabetes Mellitus = 1
Stroke or TIA = 2
Vascular disease = 1
Female sex = 1
263
What would you see on an ECG for someone in AF?
Irregularly irregular
F (Fibrillatory) waves
No clear P waves
Rapid QRS complex
absence of [isoelectric]
baseline
variable ventricular rate
264
Describe what first degree heart block is.
Occurs where there is delayed atrioventricular conduction through the AV node but every atrial impulse leads to a ventricular contraction.
A first-degree AV block is usually harmless and doesn't need any treatment. It could be suggestive of a more serious AV block in the future, so depending on the PR interval, it might be wise to avoid taking medications that could cause blocking.
265
What would first degree heart block look like on ECG?
It reflected by a prolonged PR interval (>0.20s) on the ECG, so **greater than 5 small boxes**
There is a 1/1 ratio between P waves and QRS complexes in first-degree AV block
266
Name some causes of first degree heart block. What is the management for it?
Caused by:
LEV’s disease - *idiopathic fibrosis and calcification of the electrical conduction system of the heart.*
IHD – scar tissue from myocyte death blocks conduction pathway
Myocarditis
Hypokalaemia
Management – asymptomatic so no treatment required
267
What is second degree AV block I? What characterises it?
**Also known as Wenckebach Block**
Generally caused by an AV node block, so conductions get weaker until a P wave fails to conduct down into a QRS complex, missing a beat.
At this point pacemaker cells in the ventricles kick in, and PR interval returns to normal
268
What would you see on a an ECG for someone with Second degree heart block, Mobitz type I?
a **growing PR interval** until a P wave **that does not send an electrical signal to the ventricles.**
This is followed by an absent QRS complex, after which the PR interval returns to normal before gradually increasing again until another QRS complex is absent. This cycle can keep repeating.
269
What characterises second degree Mobitz type II heart block?
This is where there is intermitted failure or interruption of AV conduction. This results in missing QRS complexes. There is usually a set ratio of P waves to QRS complexes ==> eg 3 P waves in a row that conduct to QRS, followed by a P wave with no QRS = a 3:1 block.
**The PR interval remains normal.**
There is a risk of asystole with Mobitz Type 2.
270
What are the differences between Mobitz type I and type II heart blocks on an ECG?
The PR interval may be normal or prolonged, however it is **constant in length unlike second-degree AV block Mobitz Type I (Wenckebach)** in which the PR interval progressively lengthens until a P wave is not conducted.
A second-degree type II AV block indicates significant conduction disease in this His-Purkinje system and is irreversible (not subject to autonomic tone or AV blocking medications).
271
What is third degree heart block?
No action potentials are conducting through the AV node, So **atrial depolarisations are completely unrelated to ventricular depolarisations**
Ventricles have to make action potentials on their own, so ventricular rate is slow, around 30-40 bpm
272
What would you see on an ECG for someone with third degree AV heart block?
So you would have Regular P-P intervals and Regular R-R intervals
But a **Lack of an apparent relationship between the P waves and QRS complexes.**
273
What is the management for AV blocks?
- **If stable:** observe
- **If unstable or risk of asystole**
- **First line:** atropine 500mcg IV
- **If no improvement:**
- Atropine 500mcg IV repeated
- Other inotropes (such as noradrenalin)
- Transcutaneous cardiac pacing (using a defibrillator)
- **In patients with high risk of asystole**
- **Temporary transvenous cardiac pacing** using an electrode on the end of a wire that is inserted into a vein and fed through the venous system to the right atrium or ventricle to stimulate them directly
- **Permanent implantable pacemaker** when available - *needed in 3rd Degree heart block*
274
What are the common causes of a right bundle branch block?
pulmonary embolism, cor pulmonale, ischaemic heart disease, atrial/ ventricular septal defect
275
What happens in a right bundle branch block?
The left ventricular wall depolarises as normal, but
The right ventricular walls are eventually depolarised by the left bundle branch, this occurs by a slower, less efficient pathway. ***(late activation of the right ventricle)***
276
What happens in a left bundle branch block?
Depolarisation down the bundle of His occurs only via the right bundle branch. The **septum is abnormally depolarised from right to left.**
The right ventricular wall is depolarised as normal.
The left ventricular walls are eventually depolarised by the right bundle branch, this occurs by a slower, less efficient pathway.
**It is always pathological**
277
What would a left bundle branch blockage look like on an ECG?
- Deep S wave in V1 and a tall late R wave in V6
- WilliaM: QRS looks like a W in V1 and V2, QRS looks like an M in V4-V6
When assessing whether a broad QRS complex is LBBB or RBBB, the appearances of V1 and V6 are often enough to provide the answer using the WiLliaM and MaRroW technique.
278
What would a right bundle branch blockage look like on an ECG?
- Wide, slurred S wave in V6 and as a tall late R wave in V1
- MarroW: QRS looks like an M in V1, QRS looks like a W in V5 and V6
When assessing whether a broad QRS complex is LBBB or RBBB, the appearances of V1 and V6 are often enough to provide the answer using the WiLliaM and MaRroW technique.
279
What is the pathophysiology behind ventricular tachycardia?
areas previously scarred regions of slowed conduction *due to ischaemia, or MI* can lead to rapid, recurrent ventricular depolarisation from a focus within the ventricles
280
What causes a prolonged QRS complex on an ECG?
Multiple depolarisations of the ventricles, originating not from the atria
281
What conditions do you see wide-complex QRS tachycardias?
Ventricular tachycardia,
Ventricular fibrillation
Torsades de pointes
282
How would you treat a patient with VF?
Treatment if they are haemodynamically unstable with a pulse- do a cardioversion and look for underlying cause try and solve.
Consider using antiarrhythmic medication amiodarone
If stable then use adenosine/amiodarone then cardiovert if not successful
283
What causes a QRS complex to be broad?
A broad QRS complex occurs if there is an abnormal depolarisation sequence – for example, a ventricular ectopic where the impulse spreads slowly across the myocardium from the focus in the ventricle
284
What is the pathophysiology behind Torsades de Pointes?
secondary due to long QT period
Due to long QT period, there a **longer time before ventricular repolarisation** - and in this time **spontaneous depolarisations of the ventricles can occur**
If this happens ventricles continue to **stimulate recurrent contractions without normal repolarisation** - *known as Torsades De pointes*
285
What are ventricular ectopics?
Ventricular ectopics are premature ventricular beats caused by random electrical discharges from outside the atria.
Can occur in healthy patients, but are more common in people with underlying heart conditions e.g. ischaemic heart disease or heart failure).
Can present with weird, brief palpitations
286
What do ventricular ectopics look like on an ECG?
They can be diagnosed by ECG and appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG.
287
Name some causes of prolonged QT
Long QT Syndrome (inherited)
Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)
Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)
288
What is the management of Torsades de Pointes
Correct the cause (electrolyte disturbances or medications)
Magnesium infusion (even if they have a normal serum magnesium)
Defibrillation if VT occurs
*is the asynchronous delivery of energy, such as the shock is delivered randomly during the cardiac cycle*
289
What are the 2 shockable rhythms for a cardiac arrest?
Ventricular tachycardia
Ventricular fibrillation
If it has a V, give it the D ( for Defibrillator lol)
290
What are the two non-shockable rhythms?
Asystole- when there is no electrical activity
Pulseless electrical activity
291
What condition is right axis deviation associated with?
What does it look like on an ECG?
Lead III has the most positive deflection and lead I should be negative.
Right axis deviation is associated with right ventricular hypertrophy.
292
What conditions is left axis deviation associated with?
What does it look like on an ECG?
Lead I has the most positive deflection.
Leads II and III are negative.
Left axis deviation is associated with heart conduction abnormalities.
293
What would Right atrial enlargement look like on an ECG?
Tall P wave
294
What would left atrial enlargement look like on an ECG?
Broad notched Bifid P wave
295
What Rhythm control would you do in AF?
Rhythm control: - *either pharmacological or electrical cardioversion*
- **Pharmacological: - anti-arrhythmics**
- **Flecainide or amiodarone**: if no evidence of structural/ischaemic heart disease
- **Amiodarone**: if structural/ischaemic heart disease is present
- **Electrical cardioversion:** rapidly shock the heart back into sinus rhythm
***IF HAEMODYNAICALLY UNSTABLE, DO RHYTHM CONTROL BEFORE RATE CONTROL (aka Cardioveresion)***
296
What would Hyperkalaemia look like on an ECG?
Flat P wave
Prolonged PR interval
Tall, Peaked T wave
Wide QRS
Go, Go long, Go tall, Go wide
297
What would Hypokalaemia look like on an ECG?
ST Depression,
Flat, inverted T wave
presence of a U Wave
U Wave
Comes after T wave, - *'U' waves are thought to represent repolarization of the Purkinje fibres.*
298
What is a U wave?
The U wave is a small (0.5 mm) deflection immediately following the T wave, its polarity is the same as the T wave, meaning that they will both be in the same direction
**may be a sign of hypokalemia or drug effect or toxicity**
299
What would Hypercalcaemia cause on an ECG?
Short ST segment, and Widened T wave, Shorted QT interval
300
What would Hypocalcaemia cause on an ECG?
Prolonged ST segment
Prolonged QT interval
301
What is a Delta wave? Why does it occur?
“ A delta wave is **slurring of the upstroke of the QRS complex.**
Occurs because the action potential from the SA node is able to conduct to the ventricles **very quickly through the accessory pathway**
=> QRS occurs immediately after the P wave, making the delta wave.
302
What angles of the cardiac axis are deemed to be
Left Axis deviation
Right Axis deviation
Anything less than -30 = Left axis deviation
Anything more than +90 = right axis deviation
303
What is Brugada syndrome? What happens in it
Brugada syndrome is a genetic condition characterized by abnormal sodium channel function
Brugada syndrome is a genetic condition characterized by abnormal sodium channel function
Causes
Syncope, palpitations, or nocturnal agonal breathing
Sudden cardiac arrest, often in young males during rest or sleep
Can be asymptomatic and discovered on ECG
304
What do you see on ECG in Brugada Syndrome? What is the management of it?
Investigations
ECG: Coved-type ST-segment elevation in V1-V3 (Brugada type 1 pattern), especially with provocative testing (e.g., ajmaline or flecainide challenge)
Management
Implantable cardioverter-defibrillator (ICD) for patients with prior cardiac arrest or syncope with documented arrhythmia
Avoidance of triggering factors (e.g., certain medications, fever)
Quinidine may be used in some cases to reduce arrhythmic risk
Family screening and genetic counseling
